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Chapter 34

Orbital Infections
Allan E. Wulc
Brenda C. Edmonson
Orbital and periorbital infections are the most common causes of acute orbital
inflammation and are distinguished clinically by anatomic location. Preseptal cellulitis
and periorbital cellulitis are synonymous terms that refer to superficial spreading
cellulitis without associated spread to the postseptal tissues. Orbital cellulitis, in contrast,
is an infection of the postseptal orbital tissues sometimes associated with superficial
spreading cellulitis. Both conditions are more commonly seen in children and young
adults.1,2,3,4,5,6,7 In Schramm's series of 303 cases of orbital cellulitis, 68% of patients
were younger than 9 years of age, and only 17% were older than 15 years of age.8
Interestingly, there seems to be an unexplained preponderance of left-sided orbital
infections as compared with right-sided infections.8,9,10
In the preantibiotic era, Gamble11 reported a mortality rate of 17% in patients with
orbital cellulitis. An additional 20% of survivors had loss of vision. Even now, with the
ubiquitous use of modern imaging techniques and new antibiotics, the relative ease and
rapidity of spread of contiguous infection to the cavernous sinus and the brain renders
complications associated with misdiagnosis or inappropriate therapy life threatening.
Estimates of the case fatality rate in one series suggest an improvement from 9.4% to
2%, but this mortality rate is unacceptably high, particularly in newborns in which the
mortality rate approaches 11%.11
Although these alarming figures are 10-fold less in patients with preseptal cellulitis rather
than with orbital cellulitis, preseptal cellulitis can be associated with sepsis and bacterial
meningitis and therefore is not necessarily a benign process.12,13

The discussion in this chapter focuses on the differential diagnosis, symptoms and signs,
radiologic diagnosis, and microbiology of preseptal and orbital cellulitis. Over the past
decade, the management of sinusitis has evolved. New vaccines, better imaging and new
antibiotics along with refined methods of surgery all have improved the diagnosis and
treatment of sinusitis and as a consequence, the diagnosis and treatment of periorbital
and orbital cellulitis. A rational approach to the evaluation and management of these
conditions, as well as their sequelae, is provided.
SYSTEMS OF CLASSIFICATION
Preseptal and orbital cellulitis are two distinct conditions that have different anatomic
problems at their source but often present with a similar clinical picture.
Preseptal cellulitis usually occurs in either of four clinical settings. These settings include:
(a) sinusitis, (b) bacteremia, (c) upper respiratory infection, or (d) local cutaneous
infection.14,15,16 In the latter setting, preseptal cellulitis can arise from spread of a
contiguous anterior eyelid infection such as a chalazion, local trauma resulting in
infection such as an insect bite, or a foreign body.(Fig. 1)
Fig. 1. Preseptal cellulitis in a 32-year-old woman. Swelling developed over 3 days.
Motility was preserved.

Prior to the Haemophilus influenzae type b (Hib) vaccine, the most common clinical
presentation was of a child younger than the age of 36 months with a history of
antecedent upper respiratory tract infection, otitis media, and bacteremia and usually
resulted from infection with Hib.4 However, since the introduction of the Hib vaccine,
the incidence of Hib induced preseptal cellulitis has declined dramatically with some
studies reporting up to a 90% reduction.15
Orbital cellulitis, in contrast, usually arises from spread of infection from the paranasal
sinuses. Orbital involvement occurs in 0.5% to 3% of patients with acute sinusitis.14 In a
large series of patients with orbital cellulitis, sinusitis was responsible for orbital infection
in 75% to 90% of cases.8,18,19 The ethmoid sinus is the most commonly implicated sinus
in infections that spread to the orbit in children; the frontal and sphenoidal sinuses do
not develop until age 7.20 In adults, pansinusitis often is associated with orbital cellulitis
and spread is believed to occur through the ethmoid or frontal sinuses.
In addition to anatomic proximity, several other factors predispose the orbit to the
spread of contiguous sinus infection. Dehiscences often are present in the orbital walls,
particularly in the thin-walled lamina papyracea.21,22,23 As a consequence, pus or
transudate may rupture through the thin-walled lamina into the orbit and result in
subperiosteal abscess formation. This theoretical mechanism is consistent with the
observation that most abscesses occur in the medial orbit, adjacent to the ethmoidal
sinuses.24,25,26 Posteriorly, the optic nerve within the optic canal is adjacent to the
lateral wall of the sphenoidal sinus. Dehiscences can also be present in the lateral wall of
the sphenoidal sinus along the optic canal, in approximately 6% of cases.27
Another factor predisposing the orbit to the spread of adjacent sinus infection is the free
vascular communication between the orbit and the sinuses. The orbital veins are
valveless, and flow occurs in either direction28 through the anterior and posterior
ethmoidal foramina. Increased pressure within the sinuses caused by obstruction to
mucus outflow in sinusitis may hamper venous drainage and manifest as the eyelid
edema that accompanies acute sinus inflammation. Septic thrombophlebitis can also
occur within these vessels and allow bacterial spread into the orbit.29,30,31,32,33
However, all orbital cellulitis resulting from sinus disease is not secondary to acute
sinusitis. Orbital fracture can spread existing chronic sinus infection into the orbit (Fig.
2).25,31,32,33 Mucoceles, slowly enlarging mucus-filled cysts within the sinuses that
enlarge by pressure erosion of adjacent orbital and intracranial structures, can become
infected and result in mucopyoceles that cause both cellulitis and abscess
formation.34,35,36,37
Fig. 2. Orbital cellulitis following repair of an orbital floor fracture in a 14-year-old patient
with a history of stuffy nose. There was progressive onset of diplopia, pain, and
extraocular movement limitation 2 days after surgery to the left orbit. A. Primary
position. B. Downgaze.

Approximately 15% of orbital cellulitis occurs from other sources.8 In particular,


dacryocystitis is sometimes associated with a cellulitis that may spread posteriorly into
the orbit (Figs. 3 and 4). 8 Infection can spread to the orbit from the eye, the teeth, the
middle ear, or the face. Foreign bodies, such as wood, glass, or orbital floor implants, can
cause orbital cellulitis refractory to treatment with antibiotics that requires removal of
the nidus of infection (Fig. 5). Alternatively, a granulomatous reaction may develop
around the foreign body or a cutaneous fistula may occur.25 Orbital infection has been
described after uncomplicated eyelid, strabismus, and retinal surgery.38,39,40 Rarely,
dental work or an infected dental cyst may cause orbital cellulitis through spread of
infectious phlebitis across the pterygopalatine venous plexus.41,42 Endophthalmitis
from a variety of endogenous or exogenous causes may extend extraocularly to involve
the orbit. Finally, orbital cellulitis can occur secondarily from embolic spread in subacute
bacterial endocarditis.2,3,12

Fig. 3. Neonatal dacryocystitis. Untreated lacrimal sac infection may result in orbital
cellulitis. In addition to antibiotics, probing and irrigation are required.

Fig. 4. A. Orbital cellulitis from a dacryocystitis. The dacryocystitis developed in this 43-
year-old woman who sustained multiple orbital fractures after facial trauma. B. The axial
computed tomogram shows dacryocystitis and orbital inflammation. The patient was
treated with intravenous antibiotics and a dacryocystorhinostomy.

Fig. 5. A. Orbital cellulitis from a foreign body in a 45-year-old patient who 4 days earlier
fell off a ladder and sustained a right nasal laceration. The cellulitis was treated with
intravenous antibiotics with no improvement. All imaging scans were negative. B. At
surgery, these wooden foreign bodies were removed from the right orbit.
Regardless of its anatomic site of origin, edema develops as the orbital infection spreads
within the connective tissues. Septic thrombophlebitis may ensue and increase both
edema and orbital pressure as blood flow is impeded. Congestive signs such as chemosis,
intraocular pressure, and proptosis increase. The infection may consolidate to form an
abscess. The infection, in turn, may spread through the vascular emissaries into the
cavernous sinus or intracranially, causing cavernous sinus thrombosis, meningitis, carotid
occlusion, and subdural, epidural, or brain abscess.
A spectrum of progressive infectious changes in orbital cellulitis initially was described by
Hubert30 and modified by Smith and Spencer43 and later by Chandler,29 and is useful to
the understanding of the nature of the evolution of orbital cellulitis, in classifying the
severity of infection and defining progression and management.
Stage 1 inflammation represents preseptal cellulitis. All changes that are seen on
examination are confined to the anterior eyelid tissues. Occasionally, edema may spread
secondarily posterior to the septum but does not represent the spread of cellulitis
posteriorly. Chemosis may be present, and it may even cause minimal limitation of
ocular movement.
Stage 2 inflammation represents orbital cellulitis, with leukocytosis, and often fever,
proptosis, extraocular movement limitation, and the congestive signs discussed earlier
(Fig. 6).

Fig. 6. A. Orbital cellulitis presenting in a 27-year-old man with normal visual acuity. B.
Chemosis and limitation of abduction. C. Computed tomography shows ethmoid sinusitis
on the left side.

With stage 3 inflammation, subperiosteal orbital abscess formation occurs. The globe is
often displaced and limited in the field of gaze of the abscess, which occurs concomitant
with the signs of orbital cellulitis seen in stage 2.
In stage 4 inflammation, a true orbital abscess develops. These patients have severe
proptosis, chemosis, ophthalmoplegia, and, often, visual loss.
Stage 5 inflammation represents retro-orbital spread of infection into the cavernous
sinus. In these instances, orbital signs may occur in the fellow eye and other central
nervous system signs supervene.29
SYMPTOMS AND SIGNS
PRESEPTAL CELLULITIS
Patients with preseptal cellulitis often present with a short history of painless swelling of
the eyelids. A history of previous upper respiratory tract infection, trauma, insect or
animal bite, conjunctivitis, or chalazion may be elicited.
Fever is an inconstant feature but may be present in approximately 62% of cases.12 The
eyelid characteristically is erythematous and edematous and may show signs of the
trauma, bite, or chalazion that initiated the cellulitis (see Fig. 1). The eyelid may be
painful to palpation. The superficial spreading cellulitis is confined to the eyelid and
delimited by the attachments of the orbital septum to the arcus marginalis of the orbital
rim so that infection will extend to this area and not beyond.
Rarely, the etiology of the eyelid infection may be diagnosed clinically. Necrotizing eyelid
cellulitis may be caused by erysipelas, an infection with a group A ?-hemolytic
Streptococcus, and can give rise to lid necrosis (Fig. 7).44,45 H. influenzae produces a
characteristic nonsuppurative preseptal cellulitis with a purplish discoloration of the
eyelids.46 Staphylococcal species may cause a suppurative cellulitis with abscess
formation.

Fig. 7. A. Orbital cellulitis in 58-year-old patient secondary to Group B Streptococcus with


no previous history of eyelid trauma. Exfoliation, crusting, and necrosis of skin can be
seen.

Chemosis and extraocular motility deficits are seen only occasionally and are presumed
to result from anterior edema rather than spread of infection. Vision and pupillary
examination are always unaffected by preseptal cellulitis, and proptosis and globe
displacement never are present. Therefore, in the examination of patients with
presumed preseptal cellulitis, vision, proptosis, and extraocular movements are key
distinguishing points.
ORBITAL CELLULITIS
Orbital cellulitis presents as pain, proptosis, globe displacement, double vision, and/or
vision loss (Figs. 6 and 8). Patients often have accompanying headache and malaise. In
children fever occurs with equal incidence as in preseptal cellulitis (62%),12 whereas in
adults it may be absent 66% of the time.47

Fig. 8. A. Orbital cellulitis presenting in a 7-year-old girl. B. Computed tomography shows


bilateral ethmoid and maxillary sinusitis.

Antecedent and significant past medical history may include a history of headache,
rhinitis, sinusitis, polyposis, nasal discharge, anosmia, or recent upper respiratory tract
infection. The patient may give a history of prior orbital fracture or orbital fracture
surgery with implantation of alloplastic materials. Scleral buckling procedures and
strabismus surgery have been noted to cause orbital cellulitis; thus, the patient should be
queried regarding prior ophthalmic surgery.38,39,40 The patient may also give a history
of recent dental work, specifically dental extractions.42 The patient may have had prior
surgery of the eyelids or of the facial skeleton with insertion of wires, rigid internal
fixation (miniplates), alloplastic plates, or nondissolving suture material.34
Pain is not invariably present. It is notably absent in approximately 40% of cases, even
those presenting with abscess.25
Fever is a nonspecific sign. In the presence of purulent sinusitis, pain may be present
when the affected sinus is palpated; and with ethmoid sinusitis, pain may be elicited with
pressure on the inner canthus. The sinus may not transilluminate. Mucopurulent
rhinorrhea may be present, and the ophthalmologist when possible should look in the
nose or seek the opinion of an otorhinolaryngologist.
Proptosis, chemosis, and extraocular motility deficit are the clinical hallmarks of orbital
cellulitis (see Fig. 6). Visual acuity decrease, pupillary signs, and vision loss may occur
rapidly. Rarely, if sphenoid sinusitis occurs in isolation, the patient may present with
atypical optic neuritis without proptosis or with little in the way of superficial cellulitis.48
Optic neuropathy, with the associated pupillary finding of a relative afferent pupillary
defect and optic nerve head findings such as optic disc edema, may be observed. As
orbital pressure increases, patients can show signs of retinal and choroidal arterial and
venous stasis with congestion and a picture resembling chronic vein occlusion or central
retinal artery occlusion. Hypesthesia of the nasociliary or frontal nerves is rarely seen.
Hypotony, choroidal folds, and anterior segment inflammation with hypopyon can occur
and imply intraocular spread. A dilated nonreactive pupil implies third nerve
involvement. Patients may show signs of third, fourth, or sixth nerve involvement when
the infection extends into the orbital apex.
Subperiosteal abscess formation most often is diagnosed on neuroimaging and is
indistinguishable clinically from orbital cellulitis. Signs of an abscess include displacement
of the globe away from the affected sinus and limitation of abduction and adduction,24
but these signs can occur with orbital cellulitis as well. Intraorbital abscess formation can
present in the patient who has been partially treated for an orbital infection and may
present as proptosis or globe displacement without any infectious signs or as orbital
cellulitis.25
If infection spreads posteriorly through the superior orbital fissure to involve the
cavernous sinus, additional signs may supervene. Signs of cavernous sinus thrombosis
include headache, ipsilateral hypesthesia from involvement of the ophthalmic and
maxillary division of the trigeminal nerve; third, fourth, and sixth cranial nerve palsies;
and mental status changes from confusion to obtundation. The contralateral side may
develop cranial nerve signs, periorbital edema, or cellulitis (Fig. 9).

Fig. 9. Cavernous sinus thrombosis in a 74-year-old patient with 2-day history of right
orbital cellulitis with rapidly developed obtundation and left-sided orbital changes. A.
Primary position. B. Upgaze.

DIFFERENTIAL DIAGNOSIS
Several conditions can mimic orbital and periorbital cellulitis. Most of these present as
the same constellation of symptoms and signs and often can have a similar appearance
on neuroimaging.
PRESEPTAL CELLULITIS
Conditions that may masquerade as preseptal cellulitis include allergic edema of the
eyelids, severe blepharoconjunctivitis, dacryoadenitis (Fig. 10), trauma, thyroid eye
disease (Fig. 11), leukemic infiltrates,49 blepharochalasis syndrome, and autoimmune
inflammatory disorders such as lupus.

Fig. 10. A. Bacterial dacryoadenitis. B. Computed tomography shows a mass in the left
lacrimal gland.

Fig. 11. A. Inflammatory thyroid eye disease; note bilateral eyelid retraction and
proptosis. B. Malar festoons and right eyelid retraction.

ORBITAL CELLULITIS
Conditions that may mimic orbital cellulitis include thyroid eye disease, idiopathic
inflammatory orbital pseudotumor (Fig. 12), orbital myositis,50 orbital abscess,51
ruptured dermoid cyst, necrotic intraocular melanoma or retinoblastoma,52,53 orbital
trauma, orbital foreign body, orbital vasculitis, Wegener's granulomatosis, herpes
simplex or zoster (Fig. 13), and carotid cavernous fistula. Acute-onset proptosis with
inflammatory signs in a child always should alert the clinician to the possibility of
rhabdomyosarcoma (Fig. 14).

Fig. 12. A. Idiopathic inflammatory orbital pseudotumor. Note chemosis and limitation of
abduction. There was no evidence of anterior cellulitis. B. Computed tomography
demonstrates enlargement of right medial rectus muscle.

Fig. 13. A. Herpes zoster affecting the V1 nerve and causing upper eyelid edema and
erythema.
Fig. 14. Acute-onset proptosis in 12-year-old child caused by pseudocellulitis resulting
from rhabdomyosarcoma.

LABORATORY AND IMAGING STUDIES


As a routine, white blood cell counts and at least two sets of blood cultures are obtained
in all patients who present with orbital infections. However, since the decline in Hib as an
etiologic agent, blood cultures in patients with preseptal cellulitis are less likely to yield
positive results.14,15 Cultures of the nasopharynx and conjunctiva may be obtained,
although this may not yield significant information unless a predominant organism is
present. Cultures of the leading edge of the cellulitis are performed if there is an obvious
sign of an entry wound responsible for the cellulitis. Cultures of purulent discharge may
also be helpful. Cerebrospinal fluid is obtained for culture if the patient shows central
nervous system signs or bilateral disease. Neuroimaging via computed tomography (CT)
usually is obtained in patients with orbital cellulitis in Chandler stages 3 through
5.16,54,55 However, CT may be obtained in Chandler stages 1 and 2 based on the clinical
situation, and index of suspicion of posterior infection, sinus disease, or abscess
formation. Repeat CT is also indicated if there is no improvement after 48 hours of
appropriate antibiotic treatment or if there is worsening of the clinical signs and
symptoms.16,54,55
The white blood cell count may be elevated with leukocytosis in both orbital and
preseptal cellulitis. In one study, elevated absolute white blood cell counts were seen in
children with periorbital cellulitis and bacteremia but not as frequently as in orbital
cellulitis.12 The erythrocyte sedimentation rate may be elevated. If the infection is from
?-hemolytic Streptococcus, the antistreptolysin O titer may be elevated.
If meningitis is present, the cerebrospinal fluid may demonstrate pleocytosis, increased
protein, and decreased sugar.
ULTRASOUND
Ultrasound has higher resolution (0.1 mm) when compared with CT (0.8 mm) but adds
little clinically significant information because ultrasound misses the posterior third of
the orbit and does not image the bone and sinuses.56 Ultrasound in orbital cellulitis,
however, may be useful in ruling out orbital myositis, determining the location of orbital
foreign bodies or abscesses, and following patients with drained orbital abscesses to rule
out reaccumulation.
Ultrasound findings in subperiosteal abscess can include a signal of low or medium
reflectivity adjacent to the involved orbital wall. If the abscess is intraconal, a low
reflective signal is encountered within the cone, the muscles may be thinned as they are
placed on stretch, the sclera may be thickened, or a T sign (usually associated with
orbital pseudotumor) may be seen. Ultrasound is not helpful in distinguishing
inflammatory transudate from infectious exudate or hemorrhage.
NEURORADIOGRAPHIC STUDIES
Routine skull films and polytomography have been supplanted by CT in the evaluation of
patients with orbital cellulitis.57 CT allows the clinician to differentiate a preseptal
cellulitis from an orbital cellulitis.58 If orbital cellulitis has resulted from adjacent
intercurrent sinus infection, the diagnosis can be made and the extent of the sinus
disease estimated. Sinuses may show changes of osteomyelitis with blurring of the
osseous margins of the sinuses, air–fluid levels, or inflammatory tissue within the
normally aerated sinus.59 Central nervous system complications can be assessed by
neuroimaging, and progression of disease can also be monitored.58
CT should be performed using thin-section (2–4 mm) high-resolution scanning with
multiple views of both bone and soft tissue detail.53 Axial and coronal views should be
obtained; in one-third of patients with subperiosteal abscesses, the abscess was seen in
the coronal sections only.18 Helical CT is a fairly new technology that allows increased
resolution with decreased imaging time.60 This type of scan may be especially beneficial
in children because of the ability to obtain good imaging with a shorter imaging time.60
elica He HhIntravenous contrast material is not advocated at all centers because there is
intrinsically high contrast between infectious changes and orbital fat. However, some
authors believe that it is essential to the diagnosis, and it thus remains the preference of
the individual clinician, as well as the neuroradiologist.22,59,62
With preseptal inflammation, CT demonstrates soft tissue swelling of the eyelids and
tissue adjacent to the orbital septum (Fig. 15). The orbit is not involved, and usually the
sinuses do not show evidence of inflammation. The distinction between inflammatory
preseptal cellulitis and edema cannot be made.63

Fig. 15. Computed tomography showing preseptal cellulitis of left eye. Note that all
swelling is anterior to the orbital septum.

An extraconal or intraconal mass may be present in orbital cellulitis. Proptosis also may
be visible. In particular, with intraconal involvement, proptosis is seen with obliteration
of the normal soft tissue shadows. “Patchy enhancement” of the intraconal fat in orbital
cellulitis has been described.59 The rectus muscles, particularly the medial rectus, and
the optic nerve may be thickened.58
CT is particularly useful for imaging orbital and subperiosteal abscesses. Because the
periorbit is not adherent to the orbital walls except at the suture lines, an abscess lifts
the periorbit, creating a convexity in the orbital periosteum (Fig. 16). Usually
subperiosteal abscess formation occurs adjacent to the involved sinus,25,64 but
occasionally it occurs at a remote location such as the superolateral orbit.65 Gas may be
found within a subperiosteal abscess or within the orbit, arising either from gas-forming
bacilli or free communication with sinus air or from prior trauma (Fig. 17). 57,66 CT
cannot accurately predict whether a subperiosteal mass represents exudate,
inflammatory transudate, or hematoma.67,68
Fig. 16. Computed tomography showing subperiosteal abscess formation. Note elevation
of orbital periosteum and convexity as pus elevates periorbit from the medial orbital
wall.

Fig. 17. Intraorbital gas in a 58-year-old patient with orbital cellulitis from a left frontal
sinus mucocele. Gas appears as an area of complete radiolucency on this computed
tomographic image.

A subperiosteal abscess may rupture or invade the periorbit, resulting in an orbital


abscess. This may or may not be contiguous with the subperiosteal collection on CT.
There may be gas or air–fluid levels within the mass.51,56,58,59 An orbital abscess may
present as an enhancing ringlike peripheral mass that can be either heterogeneous or
homogeneous (Fig. 18).

Fig. 18. Orbital abscess. A. Computed tomography of an orbital abscess presenting as an


enhancing intraconal mass on right side. B. T1-weighted image. C. T2-weighted image.
Note area of high signal corresponding to abscess.

Finally, CT can demonstrate intracranial involvement such as epidural or cerebral


abscess, which is better appreciated on coronal imaging.62,63 The importance of coronal
sections on CT of abscesses has been emphasized; in one series, one-third of abscesses
were seen only on coronal sections.62
However, CT also has limitations. CT of the orbits may not demonstrate the telltale signs
of orbital involvement, because the increased water content of the orbital fat may cause
only a small rise in the attenuation coefficient of the orbital fat by 5 to 10 Hounsfield
units66 at the routine window settings. The normal fat shadows within the cone may be
obliterated.67 In other series, abscesses drained at surgery were not demonstrable on
high-resolution CT.68 CT may also miss wooden orbital foreign bodies.69,70 Recent
publications have stated the relative risk of radiation-induced fatal cancer in pediatric CT
imaging.60 Although the risk was small, it was not negligible. CT should be used
judiciously in the management of pediatric orbital cellulitis, and every attempt to
minimize radiation dose should be attempted.60
Magnetic resonance imaging (MRI) is purported to be more useful than CT in the
diagnosis of preseptal cellulitis. It is less reliable at diagnosing the subtle signs of muscle
enlargement and periscleritis and thus is not as useful in differentiating orbital cellulitis
from other inflammatory orbital diseases.71 On MRI with gadolinium contrast, orbital
cellulitis may show a smearing or linear streaking of the normal fat shadows on T2-
weighted images. MRI is excellent for demonstrating localized fluid collections such as
abscesses. It is not helpful in distinguishing a transudate from an exudate, because both
appear liquid and are of low intensity on T1-weighted images and bright on T2-weighted
images (Fig. 19).

Fig. 19. Magnetic resonance image of preseptal cellulitis with anterior abscess formation.

MRI is superior to CT in the diagnosis of cavernous sinus thrombosis. T2- and proton-
weighted images show high signal luminal narrowing as well as absent flow or localized
parenchymal infarcts (Fig. 20).72 Absent flow can be demonstrated as well in the
superior ophthalmic vein in cases of carotid or cavernous sinus thrombosis.72 MRI with
gadolinium can help define these abnormalities and can detect dural invasion.

Fig. 20. Cavernous sinus thrombosis. Axial T1 image shows cavernous carotid luminal
narrowing on right and enlargement of right cavernous sinus. Note extensive sinus
disease.

MRI may be helpful in distinguishing orbital inflammatory diseases such as orbital


pseudotumor from orbital cellulitis.73 MRI is most helpful in distinguishing the diffuse
orbital form of orbital pseudotumor as well as the localized inflammatory pseudotumors
such as the myositis, periscleritis, and scleritis forms. The diffuse orbital form is most
commonly seen on MRI as a reticular pattern with isointense signals in the orbital fat in
both T1- and T2-weighted studies.73 Orbital cellulitis is best characterized by a diffuse
pattern that is isointense in T1-weighted images and hyperintense on T2-weighted
images.73
Both CT and MRI can also help in the planning of surgery and the evaluation of treatment
efficacy.
MICROBIOLOGY OF ORBITAL INFECTIONS
The organisms responsible for orbital infections often are difficult to determine, and all
cultures must be interpreted cautiously. Information can be gained from cultures of
blood, conjunctivus, nasopharyngeal tissues, an aspirate of the leading edge of the
spreading cellulitis, sinus aspirates, purulent discharge, abscess, and cerebrospinal fluid;
however, mixed infections often are seen, and normal conjunctival or nasal
contaminates can confound or obscure the diagnosis. Furthermore, patients who were
previously treated with antibiotics may have negative cultures, despite demonstrably
purulent sinus infection or abscess formation. Aerobic and anaerobic cultures should be
performed, because unsuspected anaerobes are present in approximately 50% of cases
of presumed aerobic sinusitis and are the sole organisms in 30% of cases.74
The organisms presumed responsible for orbital infections vary by patient age and
whether the infection is preseptal or orbital. Prior to vaccination for Hib, the most
common organism responsible for preseptal cellulitis in children younger than 4 years of
age is H. influenzae. In children older than 4 years of age with preseptal infections,
Streptococcus pneumoniae, Staphylococcus aureus, S. epidermidis, and mixed anaerobic
and aerobic flora predominate.2,4,5,6,7,8,12,66,75 Anaerobic organisms include
Peptostreptococcus, Fusobacterium nucleatum, and Bacteroides spp.12
In children with orbital cellulitis, the preponderant organisms isolated by sinus aspiration
are S. aureus, Streptococcus spp., and anaerobic species.5,6,12,66
In adults, S. aureus, Escherichia coli, S. pneumoniae, and mixed flora, including
anaerobes, are the most common organisms responsible for orbital
cellulitis.3,45,76,77,78,79
However, it must be noted that sino-orbital infections do not always respect these
guidelines and orbital cellulitis with a potpourri of organisms has been described in case
reports and series, including Enterococcus, Echinococcus granulosus, Pseudomonas
aeruginosa, Klebsiella spp., E. coli, Treponema pallidum,47 Eikenella corrodens,80
Actinomyces, Mycobacterium tuberculosis,47 and M. avium.
Harris et al found age to be a factor in the microbiological etiologies of subperiosteal
abscesses.81 Children less than 9 years of age are most likely to have one aerobic
organism as the source of subperiosteal abscess. Patients older than 15 are most likely to
have polymicrobial infections, including anaerobes. Patients between the ages of 9 to 14
had a tendency to have more complicated infections.81
Bacteremia tends to occur in a younger age group and in patients who have not yet had
antibiotic treatment at the time of blood culture.2 Bacteremia is less common in children
who have been vaccinated against Hib. However, in children who have been vaccinated
against Hib, the most common microbe associated with bacteremia is S. pneumoniae.15
In one series, bacteremia was present in 5% of adult patients with orbital cellulitis.8
Children younger than age 4 have impaired humoral immunity to bacteria with
polysaccharide capsules such as H. influenzae and Streptococcus spp., and thus
disseminated infections with these organisms may be seen more commonly in this age
group.82,83,84,85 In the first year of life, cellulitis from lacrimal sac infections with
Staphylococcus or Streptococcus are more common.12,20 S. aureus, and ?- and ?-
hemolytic Streptococcus spp. are the most common pathogens grown from blood
cultures in older children with preseptal cellulitis.2,6,8,12,76
Conjunctival and nasopharyngeal cultures contain mixed flora, do not correlate
accurately with blood culture results, and are believed to be misleading in orbital
cellulitis.2,4,8,9 These cultures are obtained despite this, because they may indicate a
predominant organism or a refractory organism that may explain persistent or
deteriorating clinical signs.
Cerebrospinal fluid cultures usually are positive when meningitis or other neurologic
signs are clinically apparent.8,87 In meningitis, the most frequently implicated organism
is H. influenzae.6
In the presence of preseptal cellulitis secondary to facial trauma, the yield on aspiration
of a percutaneous aspirate of the leading edge of spreading cellulitis has been described
to be as high as 51%,12 but it is very low if no site of trauma is present.8 Approximately
0.1 mL of sterile saline without preservative is injected into the outer edge of the
cellulitis and reaspirated. S. aureus and Streptococcus spp. are the most common
organisms isolated, as expected, because these organisms are among the common
causes of cutaneous cellulitis.6 Anaerobic organisms may be cultured in patients with
insect, animal, or human bites.12
Sinus aspiration through direct cannulation is perhaps the most reliable means of
obtaining cultures that are of significance in orbital cellulitis because it avoids
contamination with resident nasal flora that would render interpretation of nasal
cultures difficult. This is an otolaryngologic procedure that can be accomplished by
trephination through the antrum in the vicinity of the canine fossa.88 Studies of sinusitis
by trephination suggest that coagulase-positive Staphylococcus and ?-hemolytic
Streptococcus are the predominant aerobic organisms, but multiple bacteria, from H.
influenzae, S. epidermidis, Neisseria spp., E. coli, H. haemolyticus, pneumococcus, and
Pseudomonas, may be responsible for sinus infection.74 Anaerobic Streptococcus,
Corynebacterium, Bacteroides spp., and Veillonella are isolated in 50% of chronic
sinusitis cases, suggesting that they may play a role in sinus infection, and consequently
in orbital infections.89 It is common for multiple anaerobic organisms to be present and
coexist synergistically in orbital infections. For example, Bacteroides melaninogenicus
has an obligatory requirement of vitamin K that can be met by the metabolic activity of
other Bacteroides strains.89
The yield on culture of an abscess depends largely on whether the patient has been
pretreated. In Schramm's series, 18 of 46 abscess cultures produced no growth.8
MANAGEMENT
After appropriate workup, all periorbital and orbital infections should be treated with
broad-spectrum antimicrobial agents.90,91,92 Antibiotics may be altered after culture
results. Children with preseptal cellulitis, no orbital involvement, and who do not appear
toxic should have blood cultures drawn and can be treated with intramuscular or oral
antibiotics on a daily basis as an outpatient. If the cultures are reported negative, an oral
antibiotic should be continued to complete a 10-day course.15,16,54 Selected cases of
adult preseptal cellulitis can be managed on an outpatient basis with oral antibiotics with
frequent monitoring for progression. The duration of treatment depends on response:
patients should be treated with parenteral antibiotics until they show clear evidence of
clinical improvement as manifested by a decrease in orbital congestive signs such as
proptosis, gaze limitation, cellulitis, and edema. Intravenous therapy should continue for
a minimum of 3 days. Then oral antibiotic therapy may be instituted for a total course of
10 days to 3 weeks, depending on the severity of infection. Associated bacteremia,
however, should be treated with 7 to 10 days of intravenous therapy.
In the newborn period, staphylococcal species are the most common organisms
observed in orbital cellulitis. In children younger than 4 years of age, the most common
organisms involved in orbital and periorbital infections are S. aureus, and Streptococcus
spp. Thus, treatment in the child younger than age 4 should include coverage for gram-
positive cocci.
Antibiotic selection should be determined in conjunction with the internist or
pediatrician caring for the patient. The opinion of a subspecialist in infectious disease can
be invaluable, particularly when treating the frequently hospitalized or
immunocompromised patient, because these specialists can help determine the
presence or absence of other systemic findings, guide fluid and electrolyte therapy, and
manage any other concomitant medical problems.
Treatment regimens vary depending on whether the infection is from a cutaneous
source, the age of the patient, and the patient's culture results and immune status.
For cutaneous infections causing preseptal cellulitis, nafcillin 150 mg/kg per day every 6
hours covers most of the gram-positive organisms responsible for cutaneous infection. In
penicillin-allergic patients or those who prove to have methicillin-resistant S. aureus,
vancomycin 40 mg/kg per day in divided doses every 6 hours can be administered.
Some of the preferred antibiotics for children with orbital or periorbital cellulitis not
obviously related to a skin infection include the following.
Ticarcillin-clavulanate, which covers most gram-negative as well as -positive organisms,
including nontypeable H. influenzae, also provides excellent anaerobic coverage. The
clavulanate used with ticarcillin inactivates ?-lactamases by inactivating the active sites
of these enzymes, thus increasing the drug's microbial spectrum. Ticarcillin clavulanate is
administered in doses of 200 to 300 mg/kg per day in four divided doses.
Cefotaxime, a third-generation cephalosporin that covers all the most common sinus
pathogens with the exception of Clostridium difficile, can be given in a dosage of 80 to
120 mg/kg per day in four divided doses.
Cefuroxime, a second-generation cephalosporin, covers most staphylococci and H.
influenzae. Certain strains of Enterococcus faecalis, Serratia, Proteus vulgaris, C. difficile,
and Bacteroides fragilis are not susceptible to the drug. The dosage in children is 75 to
150 mg/kg per day in three divided doses.
In patients who are allergic to penicillin, the preferred treatment is clindamycin, 25 to 40
mg/kg every 6 hours. Clindamycin may cause a pseudomembranous colitis from
proliferation of C. difficile, as can many other antibiotics. Alternatively, chloramphenicol
50 to 100 mg/kg every 6 hours can be used. Chloramphenicol may cause both a
reversible and an irreversible bone marrow depression.
In adults who present with orbital cellulitis, the authors prefer to use cefuroxime 750 mg
to 1.5 g every 8 hours. It is effective against most gram-positive and -negative organisms
except Pseudomonas.
Alternatively, ceftriaxone 1 to 2 g/day can be given and is effective against penicillinase-
producing S. aureus, most gram-positive organisms, and most gram-negative organisms
except for Pseudomonas. Ceftriaxone also crosses the blood–brain barrier; therefore, it is
an excellent choice if there is suspicion of intracurrent intracranial infection. Methicillin-
resistant Staphylococcus and many strains of group D streptococci and enterococci,
however, are resistant.
If anaerobic bacteria are suspected, metronidazole can be added in doses of 15 mg/kg
infused over 1 hour, followed by 7.5 mg/kg over 1 hour every 6 hours after the loading
dose. Clindamycin can also be substituted, but the frequency of antibiotic-induced
diarrhea makes metronidazole a better choice. Metronidazole has not been approved for
use in children.
In patients who are frequently hospitalized, in whom an infection with methicillin-
resistant staphylococci is a possibility, vancomycin, in a dose of 500 mg given
intravenously every 6 hours, and cefuroxime can be employed. This combination of
antibiotics effectively covers most organisms, including methicillin-resistant
Staphylococcus as well as H. influenzae. S. pneumoniae resistant to penicillin and
cephalosporins is increasing; therefore, in cases where meningitis is suspected,
vancomycin should be administered.15
Fluoroquinolones often are used for the treatment of acute sinusitis.93 These antibiotics
have an expanded antibacterial spectrum that includes gram-positive and -negative
organisms as well as atypical respiratory bacteria such as Mycoplasma.94 The newer
fluoroquinolones such as moxifloxacillin (400 mg orally daily) are very active against the
respiratory tract pathogens including penicillin and macrolide-resistant strains of
Streptococcus pneumoniae.95 Fluoroquinolones are not recommended for use in
pediatric patients as first-line therapy for any infection because of the musculoskeletal
side effects.96 Fluoroquinolones have not been studied as treatment for preseptal or
orbital cellulitis.
In patients older than 9 years of age, with subperiosteal abscesses, polymicrobial
infections are the rule. Therefore, a combination of antibiotics to cover gram-positive,
gram-negative, and anaerobes is necessary. An example includes ceftriaxone with
clindamycin or metronidazole in the previously mentioned doses.14,18
Once congestive and orbital inflammatory signs diminish, oral antibiotics can be
substituted. In patients with cutaneous cellulitis, dicloxacillin 25 to 40 mg/kg per day in
four divided doses can be substituted for nafcillin. Cefaclor 40 mg/kg per day in divided
doses every 8 hours can be given, or Augmentin (amoxicillin and clavulanate potassium)
40 mg/kg per day in divided doses every 8 hours can be substituted. Oral erythromycin
40 mg/kg per day in four divided doses can be substituted if the patient is allergic to
penicillin. In anaerobic infections, metronidazole 500 mg every 6 hours can be
administered. When switching from the intravenous to the oral route, particularly when
changing antibiotics, patients must be followed closely for recrudescence.
Careful follow-up is indicated in all patients who present with orbital cellulitis. This
should include twice-daily examinations with attention to visual acuity, confrontation
visual fields, exophthalmometry, motility, and pupillary examinations. Patients may not
respond to the antibiotic regimen chosen for them because they have an abscess or a
foreign body, because they are infected with a resistant organism, because they have an
infection with an atypical organism such as Mycobacterium tuberculosis or fungus, or if
they have an inflammatory tumor rather than an infection. The authors do not hesitate
to order another CT scan if there is little improvement with treatment after 24 or 48
hours or if the patient's clinical status deteriorates.
Another measure considered useful in the medical management of orbital and preseptal
cellulitis is the use of cool compresses to reduce swelling.29 Some authors suggest the
use of warm compresses,2,76,97,98 to facilitate vascular dilation and hence delivery of
antibiotic. Nasal vasoconstrictors3,29,98 and topical antibiotics are recommended by
some,2,8,77 but others are skeptical of their efficacy.99 Head elevation may hasten the
resolution of periorbital edema.97 Patients with severe proptosis and exposure may
require lubrication of the ocular surface as well as the use of plastic wrap or exposure
bubbles to manage nocturnal exposure resulting from lagophthalmos.
The indications for surgery in orbital cellulitis include suspicion of orbital abscess or
foreign body, progression of visual loss, and extraocular motility deficit, or worsening
proptosis despite appropriate medical therapy after a 24- to 48-hour period. The orbit
should be explored to obtain gram stains and acid-fast stains and anaerobic, aerobic, and
fungal cultures. Both fresh and formalinized tissue should also be obtained if an
inflammatory orbital tumor is part of the differential diagnosis or if fungal invasion must
be ruled out.
Timing for surgical intervention is critical. In cases of orbital cellulitis without abscess
formation, in which visual acuity is 20/60 (Snellen notation), 6/15 (metric equivalent) or
less, or declines with appropriate medical management, orbital exploration should be
emergent. In cases in which the acuity is better than 20/60, the patient should be
followed serially, expectantly, and frequently while more conservative management is
initiated.
An abscess may be diagnosed at presentation or may develop with treatment. If there is
radiographic evidence of subperiosteal abscess, the need for emergent therapeutic
intervention is controversial. Some authors recommend conservative treatment,57,64,69
whereas other groups favor immediate surgical drainage, emphasizing that delayed
treatment has a higher rate of complications.8,24,25,29,51,100 In patients older than 14
years of age, the authors favor the latter approach because the risks of surgery are
negligible compared with the visual and life-threatening risks of nonintervention. In
patients 9 years of age or younger 25% of subperiosteal abscesses are likely to resolve
with antibiotic therapy alone.81 Moreover, neuroimaging may not always detect abscess
formation,68 so the authors are reluctant to be guided solely by neuroradiographic
findings.
The surgical management involves the drainage of the abscess and the involved sinus
with the restoration of normal drainage of the sinuses into the nose, usually in
conjunction with an otorhinolaryngologist. In the past, and possibly currently in certain
institutions, a subperiosteal abscess was approached and drained extraperiosteally
without entering the orbit directly, usually in conjunction with an external procedure on
the involved sinus, such as an external ethmoidectomy, antral lavage, or frontal
sinusotomy, depending on the sinus thought to be responsible for the orbital infection.8
A nasal sinusotomy was performed to facilitate drainage of the sinus. A drain was placed
to drain the involved sinus and/or the orbit and was brought out either through the
surgical wound or the nose, left in place and advanced on a daily basis. However, more
recently, because of the increasing popularity and facility of rhinologists with the
endoscopic approach, many subperiosteal abscesses are approached via an endoscopic
transnasal ethmoidectomy and are drained successfully. This procedure results in less
scarring, less inflammation, more physiologic restoration of sinus drainage than older
sinus procedures, and faster recovery.55,88,101
If an abscess has extended into the intraconal space, however, the orbit must be
entered. This can be accomplished at the time of ethmoidectomy by making incisions
into the medial periorbit, allowing the orbital fat to prolapse beyond the periosteum.
However, this approach is not advocated: the intraconal space is much more clearly
visualized using a medial or lateral orbital approach.
In patients who fail to improve after surgical drainage of abscess, a reaccumulation of
abscess, an orbital foreign body, an osteomyelitis, or an inappropriate choice of an
antibiotic may be the reason.24 These patients should be recultured, reimaged, and if
necessary, re-explored.
COMPLICATIONS
Multiple complications of orbital cellulitis can occur despite a high incidence of clinical
suspicion, improved imaging techniques, and improved intravenous antibiotics. Most
commonly, inadequately treated orbital infections can progress (e.g., orbital cellulitis can
proceed to abscess formation).
Loss of vision can occur and may result from optic neuritis;from thromboembolic lesions
to the vascular supply of the optic nerve, retina, or choroid; from rapid and sustained
intraocular pressure elevation; or, rarely, from massive proptosis, which may
mechanically distort the optic nerve.24 If light perception is lost, blindness may be
irreversible.25 However, vision has been restored in some cases with emergent surgical
treatment; thus, these patients must be diagnosed and managed expediently.100
Permanent motility defects and scarring from corneal exposure owing to proptosis and
exposure have been reported, as have perforation of the globe resulting from rise in
orbital and intraocular pressure with scleral rupture.102,103
Cerebral complications including cavernous sinus thrombosis, meningitis, carotid
occlusion, epidural abscess, subdural abscess, brain abscess, and death have been
reported.2,8,17 The use of anicoagulants in the treatment of cavernous sinus thrombosis
is still controversial because of the risk of cerebral hemorrhage.104 However, a review of
the literature suggests that anticoagulation is beneficial and that the risk of intracranial
hemorrhage from it is rare if hemorrhagic sequelae of the thrombosis is ruled out prior
to treatment with neuroimaging. The goal of the anticoagulation is an APTT of 1.5 to
2.104
FUNGAL INFECTIONS OF THE ORBIT
ASPERGILLOSIS
Aspergillus is a fungus of the Ascomycetes class that is a ubiquitous organism that
colonizes both the respiratory and gastrointestinal tracts. It rarely causes infection
except in the immunocompromised host.
Aspergillosis has four well-characterized presentations. The four presentations are
allergic fungal sinusitis, sinus mycetoma or fungal ball, acute fulminant invasive fungal
sinusitis, and chronic indolent invasive fungal sinusitis. Invasive sinusitis implies tissue
invasion with destruction of adjacent structures. Acute fulminant invasive sinusitis
presents in the immunocompromised patient as a fulminant sinusitis with rapid
progression into the orbit and cranium that produces a necrotizing vasculitis with
necrosis of sinus and nasal mucosa and bone (Fig. 21). Infection may disseminate and
produce lung, liver, and splenic invasion with an overwhelmingly poor prognosis despite
local debridement and intravenous amphotericin
B.105,106,107,108,109,110,111,112,113 Chronic or indolent invasive fungal sinusitis
usually presents in the patient with diabetes mellitus with chronic erosion through most
anatomic barriers and invasion through the orbital bones and cranium, producing orbital
signs, headache, and neurologic symptoms. The orbital signs usually result from an
orbital apex syndrome.106,107,108,109,110,111,112

Fig. 21. Invasive aspergillosis. A. Patient has postchemotherapeutic chronic myelocytic


leukemia with absolute lymphocytopenia. Computed tomography shows dense area
along medial orbit. B. This patient after exenteration of his right orbit.

Alternatively, the disease can present in the healthy host in a noninvasive form as sinus
mycetoma or allergic fungal sinusitis.106 A colony of organisms forms a mycetoma in a
sinus and gives rise to a chronic sinusitis. This type of aspergillosis is more common in
hot humid climates. These patients present with nasal congestion, postnasal drip, and
chronic sinus pain, along with frequent bouts of acute sinusitis. A mass is seen that
originates from an adjacent sinus that may have sclerotic margins and can produce an
adjacent inflammatory reaction within the orbit. This form responds well to surgical
debridement with restoration of normal sinus drainage and does not require intravenous
antifungal therapy.114 Allergic fungal sinusitis is an allergic reaction to aerosolized
environmental fungi and causes patients to suffer from headaches and nasal stuffiness.
Patients may also present with proptosis and extraocular muscle entrapment. Treatment
consists of surgical debridement and steroids without antifungals.106,109,112
Computed tomographic findings in patients with both forms of the disease demonstrate
areas that are almost metallic in density. These foci of irregularly calcified bone on CT
may be pathognomonic (Fig. 22). On MRI, these areas appeared bright on T1-weighted
imaging and have decreased signal on T2-weighted images, which may be related to the
presence of ferromagnetic materials such as iron and manganese within the fungal
concretions.115

Fig. 22. Aspergillosis. Computed tomography shows areas of extreme density of the
ethmoidal bones.

Biopsy of tissue within the orbit shows invasion of the mucosa, submucosa, and bone in
cases of invasive fungal sinusitis or a granulomatous reaction without mucosal or bone
invasion in the noninvasive form. The material within the sinuses may be yellowish,
black, or friable. Hyphae are not seen within the mucosa or bone of patients with the
noninvasive form but can be seen on routine stains of mucus. Multiple specimens should
be examined116 in a search for septate fungal hyphae of relatively uniform width that
are apparent on hematoxylin and eosin staining.
The most common effects on the orbit are cellulitis, proptosis, ptosis, and diplopia.
Invasion in both forms may produce pain. Optic nerve involvement is rare. The orbit may
be affected by contiguous spread from the sinuses, usually the ethmoid.
The treatment for aspergillosis in the immunosuppressed patient is both medical and
surgical, with antifungal agents (usually amphotericin B) and radical debridement and
sinus surgery.106,107,111 Flucytosine and rifampin with amphotericin B may be more
effective than amphotericin alone.117,118,119
Conservative debridement, intravenous amphotericin, and local amphotericin irrigation
have been described as an alternative to radical surgery.99 Five milliliters of
amphotericin B is placed in sterile water, creating a concentration of 0.25 mg/mL.
Irrigation is performed two times a day directly into the orbit through a site of entry into
the orbit or sinus.116
MUCORMYCOSIS
Mucormycosis is a fungal infection with the organisms from the genera Mucor, Absidia,
and Rhizopus100,101,102 that normally are present in air, soil, vegetable matter, skin
body orifices, manure, and bread mold.120
Most patients who develop mucormycosis have a predisposing systemic disease:
Typically the infection occurs in the diabetic patient with ketoacidosis, but it can occur in
patients with renal failure, gastroenteritis, or in those who are immunosuppressed.121
Rarely, it can occur in the normal host.124,125 An association between deferoxamine
therapy for iron or aluminum excess and mucormycosis has also been described in
hemodialysis patients with chronic renal failure, as well as in a variety of hematologic
disorders.126 It is possible that the fungus uses the iron that is mobilized by
deferoxamine to proliferate, thus facilitating invasive infection.126
Rhinocerebral mucormycosis originates as a rhinitis, parapharyngitis, or sinusitis, and
spreads by invasion of blood vessel walls, causing a necrotizing vasculitis with thrombosis
of the vascular lumina and resultant infarction. The patient typically presents with
unilateral orbital apex syndrome, including severe pain, visual loss, total
ophthalmoplegia, corneal anesthesia, and multiple cranial nerve palsies.127 Orbital
cellulitis presenting with early visual loss is one of the hallmarks of mucormycosis.72
Gangrene may occur of external periorbital tissues as well as of the hard palate and nose,
and eschar-like crusting may be observed within the nose or on the hard palate (Fig. 23).
Obstruction of the central retinal artery, ciliary arteries, and choroidal circulation can
also be seen.124,125 Brain damage may occur because of spread of infection or
infarction or occlusion of affected intracranial vessels.72

Fig. 23. Mucormycosis of the right ethmoidal sinus, with right orbital subperiosteal
abscess formation. A. T1-weighted axial image. B. T2-weighted image. Note brain
abscess.

CT shows sinusitis with or without bone destruction and is indistinguishable from other
causes of orbital cellulitis.128 MRI may show carotid narrowing, occlusion, and absent
flow in the superior ophthalmic vein (Fig. 24).72

Fig. 24. Mucormycosis. A. A 72-year-old patient with acute myelogenous leukemia and
invasive fungal sinusitis presented with orbital cellulitis. B. Involvement of hard palate
with eschar. C. Fungi in the posterior ciliary artery.

Diagnosis is made by having a large index of suspicion and obtaining specimens of nasal
turbinate, sinus, or infected orbital tissue. Large, branching nonseptate hyphae are
readily apparent on hematoxylin and eosin staining or with methenamine silver staining
(see Fig. 23). These hyphae can be grown on fungal culture.
The treatment of mucormycosis involves the control of ketoacidosis or other systemic
disease. Sinus drainage must be restored, and intravenous amphotericin B in doses of up
to 1 mg/kg per day can be administered up to a total dose of 2 to 4 g. Radical and
aggressive surgical debridement of infected tissue is advocated by most authors,
including exeneration if necessary. Surgical debridement is important because local
thrombosis caused by fungal invasion prevents amphotericin from reaching necrotic and
infected tissue.
In the patient with known infection and preserved vision, the need for exenteration and
radical surgery is more controversial, particularly if orbital biopsy does not show orbital
invasion with fungal elements. Successful outcomes have been achieved with
debridement of infected tissue without exenteration.128 In one series intravenous
amphotericin has been used successfully in conjunction with local irrigation of orbital
and sinus tissues with amphotericin B.129 Hyperbaric oxygen has been used as an
adjunctive therapy for rhinocerebral mucormycosis by treating patients with 100%
oxygen at 2.5 atm for 90 minutes for approximately 6 weeks.130
In untreated patients, rhinocerebral mucormycosis is associated with a 14% survival rate.
With amphotericin B and surgery, the survival rate improves to 57%.121 This implies
nonetheless that a significant number of patients will die of this disease and emphasizes
the need for early diagnosis and aggressive management.
REFERENCES
1. Jackson K, Baker SR: Clinical implications of orbital cellulitis. Laryngoscope 96:568,
1986
2. Watters EC, Wallar H, Hiles DA, Michaels RH: Acute orbital cellulitis. Arch Ophthalmol
94:785, 1976
3. Hawkins DB, Clark RW: Orbital involvement in acute sinusitis. Clin Pediatr 16:464, 1977

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