from the bone by collection originating in the sinuses.

A large amount of pus can

cross the subperi-…. space into the deep orbitandaccumulate as a

subperiostealabstess.

The orbit is a relatively closed compartment with limited compliance

structure formed by a complex structure of bones, …..septa, and ligaments. Thus

even a small amount of additional volume (an abscess, edema or inflammation)

can can cause a significant increase in orbital pressure that can compromise the

blood supply to vital structures in the orbit. The orbital septum is a thin, fibrous,

nonelastic sheet that is a continuation of the periorbita. It originates from the

orbital rim as the arcusmarginalis and inserts into the levatoraponeurosis.

Inferiorly, it inserts in the arca of the inferior tarsus. The tarsal plates are

connected to the bones by the fibrous medial and lateral canthal ligaments. These

limit the anterior compliance, contributing to the orbit’s junction as a closed

compartment.

The lateral extensions of the sheaths of the extraocularmusxles, the

intermuscular septa, extend from one rectus muscle to the next and from the

insertions of the muscles to their origins at the annulus of Zinn posteriorly. The

fas… between the rectus muscles posteriorly in the orbit is inland often

incomplete, which allows easy extension between the extraconal and intraconal

orbital spaces.

The communication between the vascular system of the orbit and sinuses

is another factor predisposing the orbit to spread of sinus infection. Valves are

absent in the orbital …... This network forms a rich venous plexus of free
communications predisposing the orbit to hematogenous transfixion of infection.

In the presence of acute sinusitis with increased pressure in the sinuses, reversal

of flow through & anterior and posterior ethmoidal vessels provides a route for

hematogenous transmission of the infection. Hematogenous spread also occurs

from the soft tissue of the face, …nasopharynx, pharynx, and lids. The superior

ophthalmic vein receives tributaries from the angular vein, na…..ontal veins, and

vessels originating from the ophthalmic ….. The inferior ophthalmic vein drains

blood from the ….. the orbital floor, medial wall, and lower lid.

EXAMINATION OF THE EYE, ORBIT,

AND VISUAL PATHWAY

A Basic Clinical examination of the eye and orbit should be past the of the

routine examination in head and neck infections. Non-ophthalmologists can

easily gain valuable information regarding orbital and intracranial extension of

the infection using a step-by-step evaluation of the eye. Ophthalmic consultation

may be indicated in selected … to complete the examination. If visual loss is

present, …..may be a critical factor in preventing permanent … loss.

……. Examination The external examination of the …. Provides valuable

information regarding orbital and in……….. …………………….. the position of

the eye is evaluation ………… optosis (exophthalmos or

Anterior displacement of the globe) or enophthalmos (posterior displacement of

the globe) is evaluated with a Herryexophthalmometer. Tilting the patient’s head

backwar and comparing the position of the eye on both sides …. looking from

above or below is an additional option (Figure 15-1). The eye also is evaluated for
hypoglobus (eye displaced inferiorly) or hyperglobus (eye displaced superiorly)

and lateral or medial displacement of the globe. Next, …… lid and skin are

examined for swelling, edema, erythema ….. or signs of trauma to the skin.

Pressure may be applied to the lids for evaluation of orbital pressure (by gauging

th…. ease of orbital “retropulsion”).

VisionVision (far and near distance) is examined with the patient's best

optical correction whenever possible. Vision is one of the most important early

indicators of option … nerve damage but also may be affected by many other

factors. Tearing, irritation, discharge, surface disease and other corneal problems,

change in refraction caused by pressure on the globe or metabolic problems,

vitreous opacities, and retinal problems are some causes of decreased vision.

Color vision is a more sensitive indicator for optic nerve damage. The Ishihara

color test should be performed whenever possible. Red saturation test is a less

sensitive test that compares the red saturarion between both eyes and should be

performed whenever the Ishihara color lest is unavailable. Patients with nerve

damage may describe the red color seen in the affected side as washed-out red or

brown.

Visual Fields Visual fields are important signs of optic nerve damage and

sometimes can help to localize the site of nerve injury. Computerized visual fields

are more accurate but usually are impractical in a disabled or ill patient.

Confrontation visual fields should be performed in all patients at the bedside.

Extraocular MovementsExtraocular movements are assessed in all directions of

gaze for signs of nerve damage or mechanical restriction. The lid level is
evaluated for ptosis, and the levator muscle excursion also is assessed When

ocular movement is limited, forced duction testing may be applied to differentiate

mechanical restriction from nerve

Figure 15-1 Exophthalmos or cnophihalmos becomes evident figure when

the head is tilted and the eyes are observed from below (or above) inn this

case, right exophthalmos is been.

OphthalmicConsiderations and in Oral

and Maxillofacial Infections

IftachYassur

Marc J. Hirschbein

JamesW.Karesh

The eye and orbit frequently are affected by inflammatory and infectious

processes seen by chose who per- form facial surgery. The anatomical proximity

and the common blood supply and drainage system make the orbit susceptible to

infectious processes in the soft tissue of the face, paranasal sinuses, nose, teeth,

gingiva, and nasopharynx Bacterial, viral, or fungal infections can affect the eye

and orbit by direct spread of the pathogen or alteration of die blood supply and
venous or lymphatic drainage. The ophthalmic symptoms and signs may be the

earliest manifestations of an infectious process at an adjacent location or may be a

sign of progression of die preliminary infection. Infections of the upper

respiratory tract mucous membranes also may involve the conjunctiva and cornea,

with ophthalmic manifestations the most severe. Infections of the conjunctiva may

spread to regional lymph nodes and cause symptoms remote from die eye.

Embolic spread of infections of oral and facial origin may cause severe eye

infections and even blindness. Finally, scarring and destruction of tissue caused

by infections of the face and sinuses can resultin severe ocular problems.

Surgeons who treat infections of areas adjacent to the eye must be aware of die

ophthalmic manifestations maxillofacial infections to prevent the potentially

blinding or even lethal complications.

ANATOMICAL CONSIDERATIONS

The orbit is a pear-shaped structure that tapers posteriorly; the walls are composed

of seven bones. At its entrance the orbit is approximately 35 mm vertically and 40

mm horizontally. Behind the rim the diameter of the orbit first widens and then

gradually narrows toward the apex. The orbit is composed of four walls: inferior,

superior, medial, and lateral. The distance from the rim to the apex at the inferior

wall is approximately 45 mm.

Several openings exist in the orbital walls. The optic foramen transmits the

optic nerve, ophthalmic artery and sympathetic fibers from the carotid plexus. The

superior orbital fissure transmits the superior and inferior ophthalmic veins;

oculomotor, trochlear, and abducens nerves and branches of the ophthalmic

division of the trigeminal nerve. The inferior orbital fissure transmits branches of

the maxillary division of the trigeminal nerve and venous connections between the

orbit and pterygoid fossa. Small foramina transmit the anterior and posterior

ethmoidal neurovascular complex.

All air sinuses share a bony wall with the orbit. The frontal sinus above,

the maxillary sinus below, the ethmoidal sinus medially, and the sphenoid sinus at

the apical area all have a common wall with the orbit. This close relationship

renders the orbit prone to infections originating from the sinuses.

In addition to anatomical proximity, several other factors predispose the

orbit to the spread of sinus infection. The walls of the orbit are extremely thin and

congenital dehiscence is often present. Openings often occur at the junction of the

anterior and middle third of the thin lamina papyracea or over its posterior third.

Dehiscence behind the supraorbital notch of the superior wall or at the

ethmoidomaxillary suture of the inferior wall also may be present. These areas of

dehiscence add to the preexisting foramina in the orbital walls through which

blood vessels an nerves enter the orbit.32 As a result, pus and transudate may

rupture into the subperiosteal space of the orbit. This process is exacerbated by the

increased pressure in the sinuses that is present in acute sinusitis. The apex of the

orbit is exposed to the same process when the sphenoid sinus is involved. The

periorbita is loosely attached to the bone expect at the orbital rim, the apex of the

orbit, and along suture lines; therefore the periorbita can be elevated
Pupillary Reaction Pupillary reaction may be the only method to assess optic

nerve dysfunction In noncooperative patients such as infants or unconscious

patients. In the setting of orbital infection, every pupillary abnormality should first

be attributed to damage of the ipsilateral optic nerve or oculomotor nerve. When a

history of trauma is evident, damage to the iris sphincter or globe also may change

the size and shape of the pupil. Corneal or vitreal opacities do not cause pupillary

abnormalities. Also, optic nerve damage on one side does not cause mydriasis

dilation) on the same side but causes an abnormal pupillary reaction to light if the

affected side is tested.Mydriasis usually indicates damage to the parasympathetic

fibers of the ipsilatcraloculomotor nerve.

The most valuable test to detect significant optic nerve dysfunction is the

swinging flashlight test (the relative afferent pupillary defect). A bright light is

alternately swung from eye to eye. If a relative difference in light transmission

exists between the left and right optic none (because of nerve damage), the pupils

constrict in reaction to light when shined into die healthy eye; when the light is

shined into the eye with nerve damage, the pupils dilate relative to their previous

constricted condition. This finding verifies char one optic nerve transmirs less

light than the contralateral one.

OphthalmoscopyOphthalmoscopy with a direct or indirect

ophthalmoscope is necessary to complete a thorough eye examination. Possible

findings include venous stasis manifesting as dilated, tortuous veins with or with-

out retinal hemorrhages, or central or branch retinal artery occlusion seen as

narrowing of the retinal arteries with edema of the nerve fiber layer and a cherry
red spot appearance. Optic nerve ischemia may manifest as a swollen optic disc

with or without surrounding flame-shaped hemorrhages and soft exudates.

Choroidal folds may be seen with an orbital mass pushing the globe from behind.

Septic emboli to the retina are seen as hemorrhages with a white center and

vitreous opacities. A slit-lamp examination should be performed in any case of

corneal opacity, red eye, photophobia, or vision loss.

Optic nerve evaluation includes vision testing, color vision testing,

assessment of the visual fields, pupillary reaction, and direct visualization of the

optic nerve head. Imaging also may reveal nerve compression, nerve stretching, or

thickening of the nerve. In the setting of an acute event abnormality in any of

these test findings may indicate an ophthalmic emergency and consultation is

warranted.

CONTIGUOUS SPREAD OFMAXILLOFACIAL INFECTIONS

In the ocular conditions listed in the following sections, the source of the

preliminary infection can be an adjacent head and neck site, and the eye is

affected only secondarily

BACTERIOLOGY

The organisms responsible for orbital infections of contiguous spread are the same

organisms that comprise the

Predominant Normal Flora at Various Sites

 Body Site Microbial Flora

Conjunctiva Staphylococcus epidermidis

Aerobic and anaerobic diphtheroids

Nose and S. epidermidis

nasopharynx Staphylococcus aureus

Streptococcus spp.

month and S. epidermidis, non-group A strepto-

oropharynx cocci, Streptococcus pneumoniae,

Streptococcus mitis, Streptococcus sali-

varius, nonpathogenic

Neisseria,Haemophilus, Veillonella,

Bacteroides,

Fusobacterium, Treponema, Lactobacil-

Lus, yeasts

normal flora of the sinuses, nose, oropharynx, and conjunctiva (Box 15-1) Their

frequency varies according to patient age, geographical location, and whether the

orbit or preseptal tissue is involved. Anaerobic organisms are present in the upper

respiratory tract flora and are frequent with odontogenic and sinus infections.

Mixed infections also are common.

CLASSIFICATION OFORBITAL INFECTIONS

Orbital infections are classified into five stages that generally represent degrees of

severity.
Stage 1 : preseptal cellulitis. Infection is confined to the lids and periocular soft

tissue anterior to the orbital septum. The orbit may be inflamed

secondarily but is not directly infected.

Stage 2 : orbital cellulitis with proptosis, limitations in movements, and possible

optic nerve compromise

Stage 3 : orbital cellulitis with a subperiosteal abscess

Stage 4 : orbital cellulitis with a true orbital abscess within the orbital fat.

Stage 5 : retroorbital spread of the infection into the cavernous sinus or brain.

PRESEPTAL CELLULITIS

Preseptal cellulitis is defined as superficial cellulitis of the lids and periorbita

anterior to the orbital septum. The orbital structures posterior to the septum are

not infected but may be secondarily inflamed. If the infection spreads posterior to

the septum, the condition is termed orbital cellulitis.

CausesPreseptal cellulitis occurs from three primary sources

1. Preseptal cellulitis as a result of paranasal sinusitis. This type of infection

usually occurs in children and represent the majorityofperiorbital cellulitis

cases.

Figure 15.2 Preseptal cellulitis caused by dacryocystitis in a young child

The bacteria are present mainly in the sinuses, whereas the periorbital swelling is

mostly the result of secondary inflammation and venous congestion.4,62 Blood

cultures usually are sterile.

 2. Preseptal cellulitis related to upper respiratory tract infections. In this

group of young children (<5 years of age), preseptal cellulitis occurs after

bacteremic spread from a primary focus such as otitis media or

pneumonia. Blood cultures frequently yield positive ladings. The condition

may be associated with aveningitis, and progression to orbital cellulitis is

more common. In many instances, affected children pave a history of

recent upper respiratory tract infection. Haemophilusinfluenzae is a less

significant Pathogen today but was the primary pathogen in parents

younger than 4 years before the availability of vaccination.

3. Preseptal cellulitis as a result of direct inoculation. In these children a history

of trauma to the skin, lid insect bite, dacryocystitis, conjunctivitis or chalazion

usually is present and bacteremia is usually absent (Figure 15-2). An extruding

plate or screw from previous maxillofacial surgery also can serve as the source

of the infection in preseptal or even orbital cellulitis (Figure 15-3).

Symptom and Signs Patients with preseptal cellulitis when have a brief history of

painless or tender swelling of the eyelids. The eyelid is characteristically

erythematous and may show signs of trauma, an insect lite, or a chalazion that

induced the cellulitis. Signs and …… of sinusitis or upper respiratory tract

infection

…. be present.

Fever is present in more titan half of patients but is ………pecific sign.

The eyelid may be painful to palpation the spread of the infection usually is

confined to the lid by the attachment of orbital septum to the arcus margin…..)
Sometimes the infectious agent may be diagnosed ……………. H.influenzae

typically produces nonsuppurative …….. cellulitis with a purplish discolocation

and sharp

Figure 15-3 An extruding plate in a patient with previous surgery for facil

fracture.

Figure 15-4Necotizing fasciitis as a result of dacryocystorhinostomy surgery.

Cultures grew group A p-hemolytic Streptococcus.

margins. Group A β-hemolytic streptococci may produce necrotizing cellulitis of

the lids (Figure 15-4). Chemosis may occur as a result of edema caused by the

inflammation. Proptosis, limited eye movement, and optic nerve dysfunction

typically arc not present and arc considered signs of orbital cellulitis. Extraocular

movements, proptosis, vision and color vision testing, determination of visual

fields by confrontation, and tests for pupillary function therefore arc important to

differentiate preseptal cellulitis from orbital cellulitis.

Laboratory Tests and Imaging Complete blood cell ….., blood cultures, and

computed tomographic (CT) scans of the orbits and sinuses are recommended in

all cases. Cultures from the skin, sinuses, conjunctiva, nasopharynx, and

cerebrospinal fluid usually are not indicated CT scanning should be preformed

using thin sections with axial and coronal views to exclude orbital cellulitis or a

subperiosteal abscess. CT scanning demonstrates edema of the lids and periorbital

soft tissue without orbital involvement in patients with oroseptal cellulitis. The
sinuses may show evidence of acute or chronic sinusitis. Consultation with an

otolaryngologist usually is advised if concurrent sinusitis or abscess formation is

present.

Management After blood tests and nasal cultures are obtained, most patients with

preseptal cellulitis are admitted for broad-spectrum parenteral antibiotic treatment.

Most adult patients may be treated on an outpatient basis with an oral antibiotic

and close monitoring. A CT scan should be obtained if any orbital involvement is

suspected and if sinuses are the suspected source of infection. The antibiotic agent

depends on patient age and infection site. Treatment may later be modified

according to culture results and clinical response. Amoxicillin-clavulanate (Aug-

mentin, 875 mg twice daily) is appropriate for empiric therapy. Close monitoring

for signs of orbital involvement should be performed at least once a day.

ORBITAL CELLULITIS AND ABSCESS

Orbital cellulitis implies active infection of the retroseptal soft tissue of the orbit.

The preseptal soft tissue also may be infected or secondarily inflamed. Orbital

cellulitis is a serious condition that should be quickly diagnosed and treated to

prevent associated morbidity and mortality.

The sinuses arc the source of infection in 85% of cases.60 The frequency

of orbital complications from sinus infection ranges from 0.5% to 3.9%.32

Children younger than 9 years of age represent 68ft of cases; only 17% of cases

occur in patients older than 15 years.59

Causes Orbital cellulitis is associated with paranasal sinusitis in 85% of cases.

The ethmoid and maxi liar)'sinuses are present from birch and are responsible for
57% to 75% of orbital cellulitis cases of sinus origin.21.35 The frontal sinus is

absent at birth and begins to develop at age 5 to 7 years. After its development the

frontal sinus plays an equally significant role.28.50The sphenoid sinus is present at

birth, but its clinical significance only occurs at more advanced ages. The

proximity of the sphenoid sinus to the orbital apex produces clinical signs at an

early stage.

Approximately 15% of orbital cellulitis occurs from other head and neck

sources. Spread of the infection from contiguous dacryocystitis or preseptal

cellulitis is a well-recognized cause of orbital cellulitis. Endophthalmitis may be

complicated by orbital cellulitis, but this rarely occurs because the sclera acts as

an effective barrier to extraocular spread of bacterial infections. Odontogenic

infections, maxillary osteomyelitis, and dental work (specifically, dental

extraction) are also well-known sources of orbital infection.2.18.34 Trauma can

cause orbital cellulitis by direct inoculation of the infection, promoting infection

around a foreign body, or providing the normal flora of the nose and sinuses a

direct route of ………… when a fracture is present.32 Finally, the orbit may be

Figure 15-5 A, Orbital cellulitis manifests as swollen erythematous lids. B,

Orbital cellulitis characterized by limited ocular movement, confirming the

presence of an orbital process.

infected secondarily by hematogenous seeding of the infection from a remote

source.

The organism presumed responsible for orbital cellulitis depends on patient

age and cause of the infection. In children, most common organisms include
Staphylococcus, aureus, Streptococcus spp., and anaerobes. In adults.S. ………

Escherichia colt, Streptococcus pneumoniae, and anaerobes are the most common

organisms responsible for orbital cellulitis.70H.influenzae is a pathogen that occurs

much less frequently in children since the development of the vaccination.

Anaerobes are common with human or animal bites.

Symptoms and Signs Orbital cellulitis typicallybegins with painful swelling of

the eyelid that is also erythematous and warm to the touch (Figure 15-5).

Conjunctivalchemosis is more common than preseptal cellulitis usually is more

severe, occasionally prolapsing through 1, orbital fissure (Figure 15-6). Lid

swelling may be minimal in sphenoid sinusitis, which may manifest as a posterior

orbital cellulitis and orbital apex syndrome The classic signs that Clinically

distinguish orbital cellulitis from preseptal cellulitis include proptosis, limitation

ofocular movements, pupillary dysfunction, and signs of optic nerve damage

(decreased visual acuity, visual field loss,

problems with color vision, relative afferent papillary defect and rarely optic

nerve swelling demonstrated by funduscopy). Proptosis may be prominent enough

to cause severe corneal exposure. The globe also may be displaced because of a

subperiosteal or an orbital abscess. A dilated ornonreactive pupil is the result of

damage to the oculomotor nerve or ciliary ganglion. Limited ocular movements

may result from damage to the third, fourth, or sixth cranial nerves or mechanical

restriction caused by muscle nulling or an abscess.

 Signs of optic nerve decompensation arc the result of increased orbital

pressure with compression and stretching of the optic nerve caused by the anterior

displacement ofthe globe (Figure 15-7). As the pressure within the orbit …………

the perfusion pressure, ischemia to the optic nerve orthe retina may result with

permanent damage and even blindness. This represents an ophthalmic emergency

that should be immediately addressed. Funduscopic examination may show signs

of venous stasis, central retinal occlusion, optic nerve head edema, or choroidal

folds. In rare cases the infection itself causes direct damage to the nerve tissue or

septic thrombosis of the orbital vessels (usually with mucormycosis infection).

Systemic signs are nonspecific and cannot be used to differentiate orbital

from preseptal cellulitis. These include fever, headache, leukocytosis, and

bacteremia. Symptoms and signs of the condition that led to the development

oforbital cellulitis (sinusitis, cellulitis, dental or ear infection, and trauma) also

may be present.

Differential Diagnosis Orbital cellulitis should be distinguished from several

conditions that appear in a similar manner. Preseptal cellulitis looks similar but

doesnot include proptosis, ocular motility problems, opticnerve dysfunction, or

pupillaryabnormalities. A subperiosteal or orbital abscess include globe

displacement (by the mass effect of the abscess), limited ocular motility,

insufficient re….. to …….. treatment, or worsening of local signs ……………

Figure 15-7 A, Orbital cellulitis in a middle-aged man with severe orbital

cellulitis and swelling of the brow and temporal areas The lids are very tense and

painful. Complete ophthalmoplegia was present. B, CT scan of the same patient

demonstrating the “sretched” optic nerve. C, CT scan shows severe proptosis and

tenting of the posterior sclera. The optic nerve cannot stretch any farther which

causes tethering of the anteriorly displaced globe at theinsertion of the optic nerve

and distortion of the posterior sclera.

Cavernous sinus thrombosis may be present same signs and symptoms and

sometimes can be differentiated from orbital cellulitis only by neuroimaging.

Findingssuggestive of cavernous sinus thrombosis include ophthalmoplegia

disproportionate to the amount ofproptosis, severe systemic findings, signs of

central nervous system impairment, and bilateral involvement. Findings

suggestive of orbital cellulitis include ocular adnexal tenderness and loss of

vision.

Other conditions that may mimic orbital cellulitis areidiopathic orbital

inflammation (orbital pseudotumor(Figure 15-8,A), other inflammatory conditions

(e.g., thyroidorbitopathy(Figure 15-8, B) and Wegener’s granul………. (Figure

15-8, C), orbital tumors with acute ………………… (rupturedorbital dermoid

cyst, lymphangioma, rhabdomyosarcoma[Figure 15-8. D andK]),orbital trauma or

organic foreign bodies, acute carotid cavernous ……………. (Figure 15-8, F),

fungal orbital, cellulitis (mucormycosisand aspergillosis), and rarely viral

infections such as herpes zoster ophthalmicus.61During acute stages these

conditions may be easily confused with orbital cellulitis.

Imaging Routine imaging of every patient with an orbital infection is prudent. CT

is the preferred method fororbital imaging, but ultrasonography and magnetic

reso…….. imaging (MRI) are indicted in specific conditions.

CT scanning should be performed with axial and coro…….. thinuts (2 to 4

mm). CT’s advantages include its capability to demonstrate the orbit, bones,

sinuses, and brain, and its cost-effectiveness. With orbital cellulitis the …. May be

proptotic and the orbital fat more intense compared with the other side (Figure 15-

9). The extraocular muscles usually are normal but may be thickened. CT

scanning can identify a subperiosteal abscess that is demonstrated as a convexity

in the orbital periosteum with lower …………. than bone (Figure 15-10). CT

usually cannot determine whether the subperiosteal fluid is pus, transudate,

……blood. An orbital abscess is demonstrated as a mass with the peripheral ring

enhanced with contrast. CT often can-

Figure 15-9 CT scan of a patient with orbital cellulitis demon……….. proptosis,

ethmoid sinusitis, tenting of the posterior ……….. and increased intensity of the

orbital fat on the left side.

Figure 15-10Subperiosteal abscess : CT scan of the orbits shows ……………

sinusitis with collection of subperiosteal fluid along

……………………………………… of the medial rectus muscle is

…………………………

CT scan of a patient with orbital cellulitis demon……….. proptosis, ethmoid

sinusitis, tenting of the posterior ……….. and increased intensity of the orbital fat

on the left side.

TreatmentThe following management is recommended for all patients with

orbital infections:

1. Hospital admission. Orbital infection is a potentially lethal infection that can

cause rapid deterioration in a patient’s condition, especially in small children,

Close observation in a hospital setting is always recommended.

2. Performance of blood cultures and blood cell counts. Conjunctival and nasal

cultures have limited value. A CT scan of the orbit and sinuses should be

performedwith thin axial and coronal cues. Scans should berepeated to follow

the patient’s progress if no improvement occurs within 48 hours.

3. Initiation of intravenous broad-spectrum antimicrobial treatment.Current

antibiotic recommendations include cefotaxime (50 mg/kg q6h IV) or

ceftriaxone ; (50 mg/kg q6h IV). If anaerobic infection is suspected,

clindamycin (40 mg/kg/day IV in three divided doses) may be added to the

regimen. Treatment may be modified according to the culture result.

Intravenoustreatment is given for 10 to 14 days followed by oral treatment for

a total of 3 weeks of antibiotics. Consultation with an infectious disease

specialist is advisable.

4. Daily follow-up of the patient's general condition and vital signs, white blood

cell count, lid edema, exophthalmometry, visual acuity, color vision,

confrontation,visual fields, ocular movements, and pupillary reaction.

5. Ancillarytreatment, including pain control, nasal decongestants, warm

compresses, and head elevation to reduce swelling.

Several points merit special attention. If no improvement is evident within

48 hours of appropriate treatment or worsening occurs, the clinician should repeat

imaging to look for an abscess, a cavernous sinus thrombosis, or a brain abscess.

The antibiotic coverage should be reevaluated and cultures repeated. Biopsy

sampling of the nose or sinuses should be considered to rule out

mucormycosisand other atypical pathological conditions.

Treatment of a subperiosteal abscess is controversial. In the past, immediate

drainage of all abscesses was