Orbital Infections

Infections of the orbit are uncommon, but they are potentially devastating infections that can quickly result in blindness, meningitis, or death. The emergency physician must make a rapid and accurate diagnosis and then quickly initiate therapy because visual loss is associated directly with the length of time to definitive treatment. ^[1]

The orbit is a pyramid-shaped bony space in the anterior skull that contains the globe, the blood vessels, and the intraorbital muscles and nerves. The space is bordered on its superior, medial, and inferior sides by the facial sinuses (frontal, ethmoid and sphenoid/maxillary, respectively). Note, the frontal sinuses normally develop at the age of 8 years and are not fully developed until puberty. The bony septa separating the orbit from the sinuses are thin and fenestrated, particularly in the medial orbital wall, where the lateral ethmoid bone, which also makes up the medial orbital wall, is particularly thin and porous and is named the lamina papyracea. An understanding of this anatomic relationship (see the image below) is key to appreciating the pathophysiology of orbital infections.

The anterior border of the orbit is marked by the orbital septum, a fibrous band from the external bony orbit to both eyelids (specifically from the periosteum of the orbital rim to the levator aponeurosis in the upper eyelid and to the inferior border of the tarsal plate in the lower eyelid), which effectively separates the preseptal space from the orbital space. This actually is contiguous with the periosteum that is reflected into the upper and lower lids. The posterior wall of the orbit contains the optic canal and the superior and inferior orbital fissures. The superior orbital fissure connects directly to the cavernous sinus and the intracranial space. The facial veins drain directly into the valveless superior and inferior ophthalmic veins. These, in turn, drain via many anastomoses into the cavernous sinus. The posterior wall is the source of the blood and nerve supply to the orbit.

The optic nerve (cranial nerve [CN] II) enters the orbit with the ophthalmic artery through the optic canal. CNs III, IV, and VI; the ophthalmic branch of the trigeminal nerve (CN V1); and the superior ophthalmic vein enter the cavernous sinus after exiting the orbit through the superior orbital fissure.

The superior ophthalmic vein provides the main venous drainage for the contents of the orbit. The smaller inferior ophthalmic vein exits the orbit through the inferior orbital fissure with the maxillary branch of the trigeminal nerve (CN V2) and connects with the temporal fossa.

Orbital infections develop via direct inoculation, extension from adjacent structures, and hematogenous spread. Sixty percent of these infections develop from the direct spread of sinusitis, with the ethmoid sinus being the most commonly implicated owing to its thin and porous walls (lamina papyracea).

Infections can spread from the preseptal space, particularly from preseptal (or periorbital) cellulitis in children, as well as from the pharynx, middle ear, facial skin, nose, lacrimal gland (dacryocystitis), or dentition. The ease and rapidity of such infectious spread relates to the facial venous system, which has a great number of anastomoses and is entirely valveless.

Infectious material can be inoculated directly into the orbital soft tissue secondary to trauma, surgery, or orbital foreign bodies. More rarely, orbital infections develop from hematogenous seeding secondary to sepsis or bacterial endocarditis.

Orbital infections are classified by a 5-tier system, as described by Smith and Spencer and modified by Chandler et al.

• Group I - Preseptal cellulitis
• Group II - Orbital cellulitis
• Group III - Subperiosteal abscess
• Group IV - Orbital abscess
• Group V - Cavernous sinus thrombosis

This classification system does not necessarily imply an order of disease progression; however, it helps explain the physical signs and symptoms of the various infections and helps organize treatment plans. Preseptal (or periorbital) cellulitis, which is an inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit, comprises the first group. It is the most common orbital complication of rhinosinusitis. ^[2] Orbital signs (eg, chemosis, proptosis, visual loss) are not present in this infection. Preseptal cellulitis (like many soft tissue infections of the face) may extend posteriorly, owing to the valveless communication of the facial and ophthalmic veins to the cavernous sinus, to produce one of the intraorbital infections (groups II-V).

Orbital cellulitis is an infection of the soft tissue of the orbit without abscess formation. It is a well-known complication of paranasal sinusitis, as well as periodontal abscesses, nasolacrimal infections, trauma, postsurgical infections, and rhabdomyosarcomas. Patients with this infection may develop orbital signs and symptoms (eg, chemosis, visual loss), and they often have more systemic toxicity than patients with preseptal cellulitis. Direct orbit CT scan has increased in its sensitivity over the years for diagnosing this entity. Most cases will show edema with or without microabscesses. ^{[3, 4]}

Orbital cellulitis may or may not progress to a significant subperiosteal abscess, orbital abscess, or cavernous sinus thrombosis.

Subperiosteal abscesses are collections of purulent material between the orbital bony wall and periosteum. This entity may develop in 7-9% of patients initially with orbital cellulitis or from spread of an adjacent infection, as occurs when ethmoid sinusitis spreads to the medial orbital subperiosteal space. This diagnosis is confirmed by CT scan, but it can be suspected based on physical examination. In addition to signs of orbital involvement (eg, chemosis, visual loss), limitations of ocular motility (ophthalmoplegia) and directional proptosis may be present from the intraorbital mass effect and entrapment of the extraocular muscles.

Orbital abscesses are collections of pus within the orbital soft tissue. Diagnosis is confirmed by CT scan, but the physical signs of severe exophthalmos and chemosis, with complete ophthalmoplegia, as well as venous engorgement or papilledema on funduscopic examination, are suggestive.

Multiple studies have been published documenting the accuracy, ease, and time-saving ability of emergency bed side ultrasound diagnosis of elevated intracranial pressure (ICP) via measurement of the optic nerve diameter. ^[5]  Lciterature suggests this same modality can be used in diagnosing papilledema from a non-ICP etiology. ^[6]

These infections usually are secondary to orbital cellulitis and sometimes can be differentiated from orbital cellulitis by the occurrence of the orbital apex syndrome. This syndrome is a collection of signs and symptoms consistent with organized infection in the posterior orbit (specifically, compression of the superior orbital fissure), and it is highly suggestive of group IV or V disease.

Signs include unilateral ptosis, proptosis, visual loss, internal and external ophthalmoplegia (ie, palsy of the pupillary and extraocular muscles), and CN V1 (forehead) anesthesia. Orbital abscess may or may not progress to cavernous sinus thrombosis.

Cavernous sinus thrombosis (CST) is an infectious thrombosis of the cavernous sinus and, although seen in only 1% of progressive orbital cellulitis cases, it carries a mortality rate of up to 30% in the modern antibiotic era (nearly 100% before effective antibiotic development). Typically, death is due to sepsis or central nervous system (CNS) infection. Morbidity, however, remains high, and complete recovery is rare. Roughly one sixth of patients are left with some degree of visual impairment, and one half have cranial nerve deficits. ^[7]

The cavernous sinus, a circular venous structure surrounding the pituitary gland, drains blood from both orbits. Although the incidence is low, CST is a serious complication of untreated orbital infections, and infectious thrombosis most commonly spreads from the orbit via communicating orbital veins traveling through the superior orbital fissure into the cavernous sinus. Infectious CST is characterized by headache, high fever, periorbital edema, proptosis, chemosis, and paralysis of eye movements. Once again, this diagnosis is confirmed by CT scan or MRI; however, the physical sign of bilateral posterior orbital disease is highly suggestive.

Bilateral involvement occurs because the right and left ophthalmic veins drain into the same circular contiguous sinus. Since the cavernous sinus is connected through the midline, thrombosis of one side may thrombose the other side. Complete internal and external ophthalmoplegia often is produced when thrombosis of the sinus causes palsy of CNs III, IV, V1, and the sympathetic fibers as they travel through prior to entry into the orbit. CN VI is most susceptible owing to its long course and narrow diameter. In addition, this explains the abducens nerve’s relatively high susceptibility to palsy in instances of elevated ICP and to intracavernous pathology because of its intraluminal course. Note the image below.

To fully understand CST, one must be reminded of its unique vascular connections. This dural sinus, like all dural sinuses (eg, sagittal, transverse), has no valves. Because of this, blood flows in either direction because of pressure gradients in the vascular system. Additionally, the CST receives many connections from potentially vulnerable, centrally located facial structures. Septic thrombosis can develop from infected tributary sites such as the face, nose, soft palate, tonsils, teeth, and ears. ^[8] Note that the wide use of antibiotic therapy for infections involving the stated structures has allowed an increasing emergence of sphenoid sinusitis–induced CST.

The distinction between infectious thrombosis and orbital infection alone is important because the treatment of cavernous sinus thrombosis may involve the addition of anticoagulation therapy to the antibiotic therapy. The use of anticoagulation therapy in sinus thrombosis remains controversial because of concerns with safety, as it may precipitate a hemorrhagic infarct. ^{[9, 10]} Intracranial infection or cavernous sinus thrombosis can result from any stage of orbital infections.

Mortality/Morbidity

Orbital infections may result in the following:

• Cavernous sinus thrombosis
• Brain abscess or meningitis
• Permanent vision loss

Sex

Males are affected slightly more often than females.

Age

Orbital infections are more common in persons younger than 19 years. In fact, bacteremic periorbital cellulitis most often is seen in infants younger than 18 months of age.

Orbital infections are more severe in adults.

The prognosis may include the following:

• Visual loss - Can be secondary to neurotropic keratitis, glaucoma, optic neuritis, central retinal artery occlusion, or optic nerve infection (10-33%)

• Cavernous sinus thrombosis – Usually die of meningitis or other CNS infection (30% mortality)

• Intracranial involvement (20-40% mortality)