Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000

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15 Orbital Cavity

Christoph W. Spraul and Gerhard K. Lang

15.1Basic Knowledge

Importance of the orbital cavity for the eye: The orbital cavity is the protective bony socket for the globe together with the optic nerve, ocular muscles, nerves, blood vessels, and lacrimal gland. These structures are surrounded by orbital fatty tissue. The orbital cavity is shaped like a funnel that opens anteriorly and inferiorly. The six ocular muscles originate at the apex of the funnel around the optic nerve and insert into the globe. The globe moves within the orbital cavity as in a joint socket.

Bony socket: This consists of seven bones (Fig. 15.1):

Frontal.

Ethmoid.

Lacrimal.

Sphenoid.

Maxillary.

Palatine.

Zygomatic.

The bony rim of the orbital cavity forms a strong ring. Its other bony surfaces include very thin plates of bone (see adjacent structures).

Adjacent structures: The close proximity of the orbital cavity to adjacent structures is clinically significant. The maxillary sinus inferior to the orbital cavity is separated from it by a plate of bone 0.5 mm thick. The ethmoidal air cells located medial and posterior to the orbital cavity are separated from it by a plate of bone only 0.3 mm thick or by periosteum alone. The following other structures are also located immediately adjacent to the orbital cavity.

Sphenoidal sinus.

Middle cranial fossa.

Region of the optic chiasm.

Pituitary gland.

Cavernous sinus.

Superior adjacent structures include the anterior cranial fossa and the frontal sinus. Table 15.1 lists the various bony openings into the orbital cavity and

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Anterior aspect of the left orbital cavity.

Fig. 15.1 Diagram of the seven orbital bones and the openings into the orbital cavity.

the anatomic structures that pass through them. Because of this anatomic situation, the orbital cavity is frequently affected by disorders of adjacent structures. For example, inflammations of the paranasal sinuses can result in orbital cellulitis.

The walls of the orbital cavity are lined with periosteum, which is also referred to as periorbita. Its anterior boundary is formed by the orbital septa extending from the orbital rim to the superior and inferior tarsal plates, the lateral and medial palpebral ligaments, and the eyelids.

Arterial supply: The orbital cavity is supplied by the ophthalmic artery, a branch of the internal carotid artery. The ophthalmic artery communicates with the angular artery, a branch of the external carotid artery, via the supraorbital and supratrochlear arteries.

Stenosis of the internal carotid artery can result in reversed blood flow through the supraorbital and supratrochlear arteries. This can be demonstrated by Doppler ultrasound studies.

15.2 Examination Methods 405

Table 15.1 Openings into the orbital cavity and the structures that pass through them

Venous drainage from the orbital cavity: The orbital cavity drains through the inferior ophthalmic vein into the pterygoid plexus, through the superior ophthalmic vein into the cavernous sinus, and through the angular vein into the facial veins.

15.2Examination Methods

Cardinal symptoms: Unilateral or bilateral enophthalmos (recession of the eyeball within the orbital cavity) or exophthalmos (protrusion of the eyeball) are characteristic of many orbital disorders (Table 15.2). These conditions should be distinguished from pseudoexophthalmos due to a long eyeball in severe myopia, and pseudoenophthalmos due to a small eyeball, such as in microphthalmos or phthisis bulbi.

The following list of examination techniques begins with the simple standard techniques and progresses to the difficult, more elaborate methods. As a general rule, orbital disorders require interdisciplinary cooperation between ENT specialists, neurologists, neurosurgeons, neuroradiologists, internists, nuclear medicine specialists, and oncologists.

15.2 Examination Methods 407

Visual acuity: See Chapter 1.

Ocular motility: The pattern of disturbed ocular motility can be a sign of the cause of the disorder. Causes may be neurogenic, myogenic, or mechanical (see Chapter 17).

Examination of the fundus: Retrobulbar processes can press the globe inward. This often produces choroidal folds that are visible upon ophthalmoscopy. Compression of the optic nerve by a tumor may result in optic nerve atrophy or edema. Meningiomas in the sheath of the optic nerve lead to the development of shunt vessels on the optic disk.

Exophthalmometry: The Hertel mirror exophthalmometer (Figs. 15.2a and b) measures the anterior projection of the globe beyond the orbital rim. A

Function and application of the Hertel mirror exophthalmometer.

E

B

Fig. 15.2 a The device measures the extraorbital prominence of the eye from the anterior surface of the cornea (dashed line) to the temporal bony rim of the orbit (F). The examiner (B) views the anterior surface of the cornea through a mirror (C). The extraorbital prominence in millimeters is then read off the integral scale (D). To obtain reproducible results, it is important to maintain a constant base setting in mm

(E) every time the exophthalmometer is applied.

Continued !

408 15 Orbital Cavity

Function and application of the Hertel mirror exophthalmometer (continued).

Fig. 15.2 b The exophthalmometer is placed on the lowest point of the temporal zygomatic. To avoid parallactic measurement errors, the examiner moves his or her own eye horizontally until the two integral graduations (black arrowheads on the right) align in the projection (black left arrow). Once the graduations are aligned, the examiner reads the value of the extraorbital prominence of the anterior surface of the cornea (long white arrow) on the scale (short white arrows). The examiner reads the measurement with only one eye. The examiner uses his or her left eye to read the value for the patient’s right eye and vice versa.

change in the position of the globe with respect to the orbital rim is a cardinal symptom of many orbital disorders (see Table 15.2).

The difference between the two sides is more important than the absolute value. A difference greater than 3 mm between the two eyes is abnormal. Unilateral exophthalmos is recognizable without an exophthalmometer. To do so, the examiner stands behind the patient, slightly lifts the patient’s upper eyelids, and looks down over the patient’s forehead toward the cheek.

Visual field testing: This is used to document damage to the optic nerve in orbital disorders.

Ultrasound studies: Two techniques are available for this noninvasive examination.

1.The B-mode scan (B stands for brightness) provides a two-dimensional image of orbital structures. This examination is indicated in the presence of suspected orbital masses.

15.3 Developmental Anomalies 409

2.The A-mode scan (A stands for amplitude) permits precise measurement of optic nerve and muscle thickness. This examination is indicated as a followup study in the presence of Graves’ disease (endocrine orbitopathy).

These studies may also be combined with Doppler scans to evaluate blood flow.

Conventional radiographic studies: These studies usually only provide information about the nature of bone structures, i.e., whether a fracture is present and where it is located. Smaller fractures often cannot be diagnosed by conventional radiography and require CT scans.

Computed tomography and magnetic resonance imaging: These modern examination modalities can precisely visualize orbital structures in various planes. They are standard methods for diagnosing tumors.

In the presence of orbital trauma, initial CT studies should be performed as this method can better visualize bony structures. Initial MRI scans should be performed where soft-tissue lesions are suspected.

Angiography: This is indicated in the presence of suspected arteriovenous fistulas.

15.3Developmental Anomalies

Congenital developmental anomalies affecting the orbital cavity are very rare.

15.3.1 Craniofacial Dysplasia

15.3.1.1 Craniostenosis

This clinical picture involves premature fusion of the cranial sutures. Clinical signs often include bilateral exophthalmos associated with ocular hypertelorism and exotropia (divergent strabismus). The mechanical impairment of the optic nerve is evidenced by development of papilledema and requires surgical decompression to prevent atrophy of the optic nerve.

15.3.1.1.1 Oxycephaly

Premature fusion of the coronal suture causes the orbits to become elevated, flattened, and smaller than normal.

410 15 Orbital Cavity

15.3.1.1.2 Craniofacial Dysostosis

Premature fusion of the coronal and sagittal sutures also results in a high skull and abnormally small orbits. This condition is also characterized by a wide root of the nose and a prominent chin.

Enucleation in early childhood can result in orbital hypoplasia as the globe provides a growth stimulus for the orbital cavity. Therefore the patient should promptly receive a prosthesis.

15.3.2 Mandibulofacial Dysplasia

15.3.2.1 Oculoauriculovertebral Dysplasia

Epibulbar dermoids near the limbus are present in addition to outer ear anomalies and rudiments of a branchial passage in the cheek (see Fig. 4.19).

15.3.2.2 Mandibulofacial Dysostosis

Also known as Treacher Collins’ syndrome (incomplete type) or Franceschetti’s syndrome (complete type), this anomaly of the first branchial arch is characterized by orbital deformities with antimongoloid palpebral fissures, coloboma of the lower eyelid, low-set ears, and a hypoplastic mandible with dental deformities.

15.3.2.3 Oculomandibular Dysostosis

In addition to the typical bird-like face, this anomaly may be accompanied by bilateral microphthalmos associated with cataract, nystagmus, and strabismus.

15.3.2.4 Rubinstein–Taybi Syndrome

This craniomandibulofacial dysplasia is primarily characterized by antimongoloid palpebral fissures, ocular hypertelorism, epicanthal folds, and enophthalmos. Cataracts, iris colobomas, and infantile glaucoma have also been described.

15.3.3Meningoencephalocele

Incomplete fusion of the cranial sutures in the orbital region can lead to evaginations of dural sac with brain tissue. Clinical findings occasionally include pulsating exophthalmos or, in extreme cases, a tumorous protrusion.

15.3.4Osteopathies

Many of these disorders can produce orbital changes. The most common of these diseases include Paget’s disease of bone, dysostosis multiplex (Hurler’s syndrome), and marble-bone disease of Albers-Schönberg in which compressive optic neuropathy also occurs.

15.4Orbital Involvement in Autoimmune Disorders: Graves’ Disease

Definition

Autoimmune disorder with orbital involvement frequently associated with thyroid dysfunction. Histologic examination reveals inflammatory infiltration of the orbital cavity.

Epidemiology: Women are affected eight times as often as men. Sixty per cent of all patients have hyperthyroidism. Ten per cent of patients with thyroid disorders develop Graves’ disease during the course of their life.

Graves’ disease is the most frequent cause of both unilateral and bilateral exophthalmos.

Etiology: The precise etiology of this autoimmune disorder is not clear. Histologic examination reveals lymphocytic infiltration of the orbital cavity. The ocular muscles are particularly severely affected. Fibrosis develops after the acute phase.

An autonomous adenoma of the thyroid gland is not associated with Graves’ disease. Some patients with Graves’ disease never exhibit any thyroid dysfunction during their entire life.

Symptoms: The onset of this generally painless disorder is usually between the ages of 20 and 45. Patients complain of reddened dry eyes with a sensation of pressure (symptoms of keratoconjunctivitis sicca) and of cosmetic problems. Ocular motility is also limited, and patients may experience double vision.

Diagnostic considerations: Cardinal symptoms include exophthalmos, which is unilateral in only 10% of all cases, and eyelid changes that involve development of a characteristic eyelid sign (Table 15.3 and Fig. 15.3). Thickening of the muscles (primarily the rectus inferior and medialis) and subsequent fibrosis lead to limited motility and double vision. Elevation is impaired; this can lead to false high values when measuring intraocular pressure with the gaze elevated.

Eyelid flutters when closed

Patient with Graves’ disease, more severe in the left than in the right eye.

Fig. 15.3 Typical signs include exophthalmos, which here is readily apparent in the left eye, retraction of the upper eyelid with visible sclera superior to the limbus (Dalrymple’s sign), conjunctival injection, and fixed gaze (Kocher’s sign).

The tentative clinical diagnosis of Graves’ disease is supported by thickening of the extraocular muscles identified in ultrasound or CT studies

(Fig. 15.4). The further diagnostic work-up requires the cooperation of an internist, endocrinologist, and radiologist.