▃Anatomy of the Orbit

The orbit is a pear-shaped bony cavity which contains the eyeball, extraocular muscles, nerves, vessels, and connective tissue to support all orbital structures. Anteriorly, the orbit is limited by the orbital septum which separates the orbit from the eyelid. The orbit is formed by seven bones (Fig. 22.1):

•Ethmoid bone.

•Frontal bone.

•Lacrimal bone.

•Maxillary bone.

•Palatine bone.

•Sphenoid bone.

•Zygomatic bone.

■Walls and Relations of the Orbit

The average volume of bony orbit is approximately 30 ml. It has four walls which converge posteriorly toward the apex and optic canal.

Orbital Roof

It slopes backward and downward toward the apex. It separates the orbit from frontal sinus anteriorly and anterior cranial fossa posteriorly. It is formed by two bones: orbital plate of frontal bone (main) and lesser wing of the sphenoid bone (small contribution at the apex of the orbit).

Applied Aspect

•Lacrimal gland fossa is located in the superotemporal aspect of roof. So, globe will be displaced inferonasally in the lacrimal gland tumor.

•A defect in orbital roof results in transmission of cerebrospinal fluid (CSF) pulsation to the orbit which may cause pulsatile proptosis.

Lateral Orbital Wall

It is formed by two bones: Zygomatic bones (anteriorly) and greater wing of the sphenoid bone (posteriorly).

Applied Aspect

Lateral wall only protects the posterior half of the globe; so, anterior half of the globe is vulnerable to lateral trauma.

Orbital Floor

It is the shortest of the orbital walls. It is formed by three bones: maxillary bone (main), zygomatic bone (forms anterolateral portion), and palatine bone (lies at posterior extent of the floor).

It is separated from the roof of maxillary sinus and lateral wall by inferior orbital fissure. Floor is traversed by infra orbital groove which is bridged over with a thin lamina of bone to form infraorbital canal, which lodges the maxillary division of trigeminal nerve and maxillary artery. These exit just below the central orbital rim at the infraorbital foramen.

Applied Aspect

•The posteromedial portion of the maxillary bone is relatively weak (just medial to the infraorbital canal), which is the most common site for “blowout” fractures, and may damage the maxillary division of the trigeminal nerve, resulting in numbness of lower lid, cheek, side of nose, upper lip, and upper teeth.

•As the orbital floor forms the roof of maxillary sinus, so maxillary carcinoma invading the orbit may displace the globe upward.

Medial Orbital Wall

The medial walls of the orbits are approximately parallel to each other. It separates the orbit from the ethmoid sinus. It is formed by four bones:

•Ethmoid bone: The medial wall is composed largely of the thin and fragile lamina papyracea of the ethmoid bone.

•Sphenoid bone: The body of sphenoid bone completes the medial wall posterior to ethmoid bone.

•Lacrimal bone: It is anterior to the ethmoid bone which forms the posterior half of lacrimal sac fossa and contains posterior lacrimal crest.

•Maxillary bone: The orbital process of maxillary bone joins the lacrimal bone in the midportion of the fossa. It is a thick bone and forms a medial part of the inferior orbital margin. The anterior lacrimal crest blends with the inferior orbital margin.

Applied Aspect

•Being paper-thin and exceptionally fragile, lamina papyracea is a frequent site of fracture in the orbital trauma.

•Lamina papyracea is breached easily during transnasal ethmoid sinus surgery.

•Lamina papyracea offers little resistance to expanding ethmoid sinus mucoceles and commonly transmits inflammation and infections from the ethmoid sinus into the orbit. Orbital cellulitis is, therefore, common secondary to ethmoidal sinusitis.

•During lacrimal bypass surgery (DCR), entrance into the nose can be achieved easily by applying pressure on the lacrimal portion of the fossa.

■Apertures of Orbit

The orbit contains inferior orbital fissure, superior orbital fissure, and optic foramen, each of which contains structures that are crucial to normal eye functioning.

Inferior Orbital Fissure

It separates lateral wall from the floor of orbit. At orbital apex, it joins the superior orbital fissure. It transmits inferior ophthalmic vein to communicate with the pterygoid venous plexus. It also transmits maxillary division of the trigeminal nerve and branches from the pterygopalatine ganglion.

Superior Orbital Fissure

It is bounded by greater and lesser wings of sphenoid bone. It transmits the following structures from the cranium to the orbit:

•The lacrimal nerve, frontal nerve, trochlear nerve, and superior ophthalmic vein through superior portion of fissure.

•Superior and inferior divisions of III nerve, abducens (VI) nerve, nasociliary nerve, and sympathetic fibers through the inferior portion of the fissure.

Optic Foramen

It is located in the lesser wing of sphenoid bone and transmits optic nerve, ophthalmic artery, and its sympathetic plexus. The dural sheath of the optic nerve is adherent to the walls of the optic foramen, so intraorbital and intracranial circulations are interconnected.

Thus, inflammation of superior orbital fissure and apex may result in ophthalmoplegia and obstruction to venous outflow as in Tolosa–Hunt syndrome (Fig. 22.2).

■Connective Tissue System of Orbit

It supports all orbital structures and includes:

•Periorbita.

•Orbital septal system.

•Tenon’s capsule.

The orbit is lined with periosteum. At the inner surface of the periosteum are multiple layers of orbital connective tissue (orbital fascia) which lines various intraorbital structures. Together, this complex layer is known as periorbita. Within the orbit, the periorbita stabilize anatomical structures. At the orbital rim, the inner layer of connective tissue system separates from periosteum and extends into the eyelids as the orbital septum. Thus, the septum represents the anterior most boundary of the orbital compartment. Orbital fascia is a continuous tissue, the extraocular muscles do not perforate this fascia but invaginate it, and the fascia is reflected from their surface. The fascia covering the eyeball (except over the cornea) is known as Tenon’s capsule (fascia bulbi). Tenon’s capsule begins at the perilimbal sclera anteriorly, where it is adhered firmly to episcleral, and extends around the globe to the optic nerve where it blends with dural sheaths and sclera. In the lower part of the orbit, Tenon’s capsule is condensed and forms a hammock on which the eyeball rests, which is called the suspensory ligament of Lockwood.

■Blood Supply of the Orbit

Arterial supply: Mainly ophthalmic artery.

Venous drainage: Orbit is drained by superior and inferior ophthalmic veins into the cavernous sinus (Fig. 22.3).

Lymphatics: There are no lymphatics in the orbit.

■Surgical Spaces of the Orbit

From the surgical point of view, there are four self-contained spaces. The inflammatory processes tend to remain within the space affected. Therefore, each space must be opened separately. These spaces are as follows (Fig. 22.4):

•Subperiosteal space is a potential space between the bones of orbital wall and the periorbita.

•Peripheral space is the space between periorbita and extraocular muscles joined by fascial connections.

•Central space is cone-shaped space enclosed by the muscles (muscular cone) and their inter muscular septa.

•Tenon’s space is a space around the globe between sclera and Tenon’s capsule.

Applied Aspect

The peripheral space is the site for peribulbar anesthesia, and proptosis produced due to tumors in this space is eccentric. The central space is the site for retrobulbar anesthesia, and proptosis produced due to tumors in this space is axial.

▃Clinical Features and Investigations in Orbital Diseases (OP2.7, 2.8)

The main features of orbital diseases are pain, proptosis, diplopia, visual impairment, and enophthalmos. Investigations of orbital lesions are listed in Flowchart 22.1.

Plain X-rays highlight bony disorders and are taken in different views (Table 22.1).

■Computerized Tomography Scan (CT Scan)

Its main advantage is its ability to take combination of axial, coronal, oblique, and sagittal sections of the orbit, which enables a space-occupying lesion within the orbit to visualize in three dimensions. Its main disadvantage is its inability to distinguish between pathological soft tissue masses.

■Orbital Ultrasonography

B-scan ultrasonography produces a two-dimensional picture of orbital structures. It requires a probe functioning at lower speed (generally 5 mHz) for greater penetration into the orbit. It gives clear delineation of soft tissues and is less useful in the evaluation of bony lesions.

■Magnetic Resonance Imaging

It generates images without the use of ionizing radiation. It images soft tissues not only within the orbit but also within the globe. It is contraindicated in the presence of magnetic foreign body or patients with pacemaker.

■Demonstration of Orbital Vascular System

Vascular anomalies in the orbit/within the cranium and vascular tumors in the orbit require angiography.

■Histopathological Examination

The biopsy material is obtained under CT and ultrasound guidance. It may be fine needle aspiration biopsy or excisional biopsy.

▃Proptosis (OP2.6)

An abnormal protrusion of eyeball beyond the orbital margin, with the patient looking straight ahead, is termed as proptosis or exophthalmos.

The term exophthalmos is reserved for protrusion of eyes secondary to thyroid diseases, and the term proptosis is used for protrusion of eyeball due to all other causes.

Normal position of eyeball: Normally, the apex of cornea does not protrude beyond the plane of orbital margins. If a scale is put vertically on the middle of the upper and lower margins of the orbit, it just touches the closed lids over the apex of cornea (Fig. 22.5). The position of two eyeballs is almost always symmetrical. Causes of proptosis are tabulated in Table 22.2.

■Classification

Proptosis can be classified as follows:

•On the basis of onset:

◊Acute.

◊Insidious.

•On the basis of direction:

◊Axial.

◊Eccentric.

•On the basis of laterality:

◊Unilateral.

◊Bilateral.

•On the basis of etiology: It may be due to:

◊Inflammation.

◊Circulatory disturbances.

◊Trauma.

◊Orbital cysts.

◊Orbital tumors.

◊Endocrine disorder.

◊Developmental disorder.

◊Disorders of paranasal sinuses.

On the basis of direction, proptosis may be axial or eccentric. The direction of proptosis may indicate the possible pathology. In axial proptosis, the eye is pushed directly forward, which is caused by space-occupying lesions within the muscle cone (central space), for example, optic nerve tumors and cavernous hemangiomas. Eccentric proptosis is caused by the extraconal lesions, that is, the lesions outside the muscle cone. The eye is displaced in opposite direction to the site of space-occupying lesion (Table 22.3).

■Clinical Evaluation

The objective of clinical evaluation is to determine the probable etiology, planning of imaging, and plan of management. It includes history, examination, and investigations.

History

It includes the following:

•Age of onset.

Proptosis in children is usually caused by:

–-Dermoid cysts.

–Capillary hemangioma.

–Optic nerve glioma.

–Rhabdomyosarcoma.

–Neurofibromatosis.

–Leukemias.

Proptosis in adults is caused by:

–Cavernous hemangioma.

–Mucocele of sinuses.

–Meningiomas.

–Metastases from breast, lung, and gastrointestinal tract.

–Nature of onset.

Acute onset: A rapidly increasing proptosis in a child may be due to orbital cellulitis, rhabdomyosarcoma, and neuroblastoma. An adult acute onset of proptosis associated with pain suggests pseudotumor.

Insidious onset: A gradually increasing proptosis occurs in the presence of slow-growing tumors such as meningiomas.

•Duration: The patient is asked about the time course of the disease. The disease may be:

◊Acute: If the time course of the disease is hours to days.

◊Subacute: If the time course of the disease is 1 to 4 weeks.

◊Chronic: If the time course of the disease is more than 1 month.

•Progression: Ask the patient how the symptoms have developed overtime. Conditions may be acute (e.g., infection) or chronic (e.g., lacrimal adenoma).

•Associated symptoms: History of visual loss, pain, and diplopia is taken.

Examination

It includes the following:

•Inspection.

•Palpation.

•Auscultation.

•Visual acuity.

•Ocular movements.

•Pupillary reactions.

•Fundus examination.

•Measurement of proptosis.

•Examination of paranasal sinuses.

•Systemic examination.

Inspection

Objectives of inspection are:

•Rule out the possibility of pseudoproptosis and enophthalmos of opposite eye (Table 22.4).

•Ascertain the laterality (unilateral or bilateral) of proptosis.

•Ascertain the type of proptosis (axial or eccentric).

•Look for pulsations of the eye which are caused by:

◊A defect in orbital roof through which CSF pulsation is transmitted to the orbit. It may be congenital (as in neurofibromatosis) or acquired (as in trauma).

◊Arteriovenous (AV) communication: Dilated corkscrew epibulbar vessels may be found in AV malformations.

Look for increase in proptosis on Valsalva maneuver or on bending forward. These maneuvers may increase the proptosis in vascular lesions such as orbital varices.

Palpation

Observe the following points during palpation:

•Compressibility: Push the normal and then the proptosed eye gently back into the orbit with the fingers. If resistance is felt during retropulsion, it suggests the presence of a tumor or thyroid ophthalmopathy.

•Orbital thrill: Orbital bruits are vibrations resulting from turbulent blood flow. Although usually heard with the stethoscope, such sounds may occasionally also be palpated as a thrill.

•Presence of mass.

•Orbital rim: Feel whether the finger can be insinuated between orbital rim and globe? Palpation of orbital rim may reveal erosion or a mass.

•Regional lymph nodes.

Auscultation

A bruit is detected by auscultating the orbit with the bell of a stethoscope. It is present with pulsations in the carotid-cavernous fistula. Both pulsation and bruit can be diminished or abolished by compressing the ipsilateral carotid artery in the neck.

Visual Acuity

Visual acuity may be impaired in orbital lesions due to:

•Optic nerve compression.

•Exposure keratopathy.

•Choroidal folds involving posterior pole changing the refractive status.

The retrobulbar lesion can compress the optic nerve in the absence of significant proptosis. A marked impairment of vision with minimal proptosis is suggestive of optic nerve glioma in children.

Ocular Movements

The restricted ocular movements may be caused by:

•Thyroid ophthalmopathy involves inferior rectus muscle, causing its fibrosis and restriction of elevation.

•Restrictive myopathy.

•Blowout fracture.

•Neurological lesion.

Forced duction test is conducted to differentiate the defective ocular movements due to fibrosis from a neurological lesion. The muscle of the involved eye to be tested is grasped with toothed forceps under topical anesthesia. The difficulty in moving the globe (in the field of action of muscle) with the forceps indicates fibrotic contracture as in thyroid ophthalmopathy. In case of palsy due to neurological lesion (III nerve palsy), no resistance will be encountered.

Pupillary Reactions

The pupillary reactions may be slow reacting or absent which indicates the optic nerve involvement.

Fundus Examination

During fundus examination, one should look for:

•Optic disc: The optic disc may show edema or pallor.

•Choroidal folds: These may occur in orbital tumors or thyroid.

•Venous engorgement.

Measurement of Proptosis

The normal distance between the lateral orbital rim and the apex of cornea is usually less than 20 mm. A difference of >2 mm between the two eyes or a reading of ≥ 21 mm is regarded as abnormal. The amount of proptosis is measured by Hertel’s exophthalmometer or with a plastic rule placed on the bone at lateral canthus (Fig. 22.6).

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