14
Fig. 22. (A) Coronal T1 weighted image (WI) demonstrates a mildly hyperintense juvenile nasopharyngeal angiofi-
broma (JNA) in the left nasal cavity (arrow). (B) On axial post contrast T1WI the JNA demonstrates enhancement (arrow).
in combination with surgery.69 Recurrence has
been noted to occur in 20% to 50% and postop-
erative radiation therapy can be effective in de-
laying or preventing recurrence.65,67,70,71 Risk
factors for recurrence include younger age at
diagnosis, larger tumor size, and higher stage
lesion.71
Fig. 23. Angiographic image shows a juvenile naso- SUMMARY
pharyngeal angiofibroma with intense tumor blush
secondary to vascularity (arrow). The diagnosis of vascular lesions of the head and
neck should be directed by classifying the le-
sions as tumors or malformations and by deter-
mining their flow characteristics (Box 6).
Location of the lesion is key when differentiating
between vascular neoplasms. US is an appro-
priate screening tool; MRI is often used to
confirm the diagnosis. CT can be used for further
characterization of the lesion, particularly when
there is bony involvement. In many cases,
vascular lesions grow to be extensive. In these
cases, percutaneous sclerotherapy or emboliza-
tion therapy can be employed to aid in surgical
resection.
Fig. 24. Angiographic image after liquid emboliza- Box 6
tion shows no residual tumor blush (arrow). What the referring physician needs to note
Ultrasonography is a high-value screening
method for evaluating superficial vascular
lesions.
MRI is the most important modality for deter-
mining lesion extent and its involvement with
soft tissues.
Computed tomography should be used judi-
ciously, but is integral in evaluating bony
involvement.
Imaging of Vascular Lesions 15
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Imaging of Head and Neck
Emergencies
Justin L. Brucker, MD, Lindell R. Gentry, MD*
KEYWORDS
Emergency radiology Head and neck infection Imaging
KEY POINTS
The anatomy of the head and neck contains very few structures that could be considered expend-
able and, consequently, is exceptionally intolerant to infection, inflammation, and injury.
Acute pathologic processes in this body region, therefore, tend to result in significant suffering,
functional impairment, or life endangerment if the diagnosis is missed or treatment is delayed.
Many emergent processes within the cervical region also need to be considered for their possible
impact on structures within the head and chest, into which there are many routes for potential
communication.
In the emergent setting, computed tomography (CT) is the favored imaging option because of its
rapid image acquisition and superior delineation of the airway and osseous structures.
On the other hand, MR imaging provides more robust information regarding complex soft tissue
structures that may be difficult to distinguish on CT.
However, any prolonged radiologic examination should only be undertaken in patients who
possess a protected airway and are medically stable enough to tolerate the duration of the scan.
This added step of preimaging clearance should entail a review of the patients’ presenting symp-
toms and past medical history, which will also help to refine the study protocol and provide a clinical
context in which to interpret the images.
INTRODUCTION: “CRIMES AGAINST that cause loss of function, (3) conditions that incite radiologic.theclinics.com
ANATOMY” severe pain or distress, or (4) any situation that can
lead to the aforementioned conditions if not identi-
If not for the thorough coverage of subject matter fied early or acted on quickly. With that being said, it
provided by the other articles of this book, the takes little imagination to see how just about any
authors’ one section, dedicated to various medical acquired abnormality of the head or neck has the
emergencies of the head and neck, may have read potential for being declared an emergency on pre-
something like an endlessly long police report sentation; in reality, this is becoming increasingly
inspired by an episode of “Head and Neck Imag- more common, according to current fashions in
ing’s Most Wanted.” Admittedly, there are many modern clinical practice. It is important to keep in
topics that would have been appropriate to include mind that, when dealing with the vital delicate anat-
under this heading; but for the sake of brevity, the omy of the head and neck, even minor violations
authors limits the discussion to the culprits that he can lead to serious disability and unnecessary
found either most offensive or intriguing. suffering, especially when inaccurately interpreted
or missed altogether. It is by the same token that
When one sits down to consider what actually relatively small transgressions may be promoted
constitutes an emergency in this region of the to the level of heinous criminal activity, should
body, any of the following situations may qualify: they occur in a sacred and vulnerable location.
(1) conditions that are life threatening, (2) conditions
Justin L. Brucker is the primary author in this article.
Head and Neck Imaging, Department of Neuroradiology, University of Wisconsin Hospital, University of
Wisconsin, E1-311 CSC, 600 Highland Ave, Madison, WI 53792, USA
* Corresponding author.
E-mail address: [email protected]
Radiol Clin N Am 53 (2015) 215–252
http://dx.doi.org/10.1016/j.rcl.2014.09.007
0033-8389/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
216 Brucker & Gentry
Take, for example, the act of littering in a nature (see Figs. 1 and 2; Figs. 3–8), given its many attrac-
preserve or smoking cigarettes in the Sistine tive features, which include: fast speed of image
Chapel (though from a head-and-neck standpoint, acquisition, large field of view (FOV), high spatial
too, one should avoid smoking altogether). resolution, relative insensitivity to patient motion,
ability to provide reformatted images from a single
In addition to the authors’ coverage of head and data acquisition, wide availability of the technology,
neck emergencies, this article includes some of and ease of technical use. In the emergent setting,
the necessary discussion about the relevant anat- these highly desirable properties should outweigh
omy and imaging techniques, though mostly in the any concerns one may have about the long-term
context of a specific disease process being effects of radiation exposure, especially if one
presented. adheres to standard imaging practices and keeps
track of CT dose reports (basic radiologic hygiene).
APPROACH TO HEAD AND NECK IMAGING Furthermore, the ongoing evolution of widely avail-
TECHNIQUES able low-dose reconstruction algorithms and
improvements in detector technology continue to
Conventional radiography plays little role in the diminish the radiation cost of CT imaging. Of note,
evaluation of patients with head and neck emer- we must always take care not to let exuberant
gencies. The anatomic information provided is dose-limiting practices sacrifice vital diagnostic
usually insufficient for diagnosing and managing information from the scan; a safe scan by definition
these conditions (Figs. 1 and 2). Computed tomog- should not facilitate a radiologist in readily missing
raphy (CT) remains the foremost radiologic tool a critical finding.
for imaging the head and neck in the acute setting
Fig. 1. Acute supraglottitis and laryngitis: (A) Lateral radiograph demonstrates enlargement of the suprahyoid
and infrahyoid epiglottis (white arrow). Sagittal (B) and axial (C, D) Computed tomography scans also reveal
edema of the epiglottis (white arrow), aryepiglottic folds (black arrows), and mucosal lining of the subglottic
larynx (white arrowheads).
Imaging of Head and Neck Emergencies 217
Fig. 2. Penetrating orbital trauma: Male psychiatric patient with a history of visual hallucinations now presenting
with blurry vision following self-inflicted penetrating orbital trauma. Lateral (A) and anteroposterior (B) radio-
graphs demonstrate a penetrating orbital foreign body (fork) extending into the inferior aspect of the right orbit
just above the orbital floor. These images do not provide any information about soft tissue injury to the orbital
contents. Axial (C, D) and coronal (E) computed tomography scans reveal a normal appearance of the globe but
ill-defined hemorrhage (curved arrow) and air (white arrows) within the right inferior oblique muscle. Note the
normal appearance of the left inferior oblique muscle (white arrowhead).
Fig. 3. Penetrating intraocular foreign body, lens dislocation: Axial (A) and oblique sagittal (B) CT scans demon-
strate a metallic foreign body (black arrow) near the inferior aspect of the sclera within the globe. There is
marked widening of the anterior and posterior chambers of the globe with subtle hemorrhage (hyphema)
(open arrows) and dislocation of the lens (black arrowheads).
218 Brucker & Gentry
Fig. 4. Penetrating intraocular and intraorbital foreign bodies, intraorbital hemorrhage, lens dislocation: Axial (A,
B) and oblique sagittal (C) CT scans demonstrate multiple intraocular and intraorbital glass fragments (black arrow-
heads) in a patient ejected through the windshield of an automobile during a motor vehicle accident. Intravitreal
(open white arrows) and anterior chamber (hyphema) hemorrhage is present. There is rupture of the left globe as
indicated by its abnormally small size. There is traumatic fragmentation of the left lens (dashed white arrows).
Fig. 5. Blunt central midface trauma with medial canthal ligament disruption, traumatic telecanthus: CT scans
(A, B) of 2 different patients who experienced severe central midface trauma resulting in periorbital contusion,
epiphora, and widening of the intrapupillary distance. The scans demonstrate multiple fractures of the central
midface including avulsion of the anterior lacrimal crests (white arrows) from their attachments indicating disrup-
tion of the medial canthal ligament complex. Fractures also involve the lacrimal sac fossa (curved white open
arrows) explaining the presence of epiphora.
Imaging of Head and Neck Emergencies 219
Fig. 6. Medial and inferior orbital wall blowout fractures, ocular rupture: Axial (A, B) and oblique sagittal (C) CT
scans reveal depressed fractures of the medial (white open arrows) and inferior (curved white open arrows)
orbital walls following blunt orbital trauma. There is obvious rupture of the globe indicated by a wrinkled,
notched (crenated) appearance (black arrowheads) and extensive intravitreal hemorrhage. There is evidence
of enlargement and hemorrhage within the anterior chamber of the orbit (hyphema) (curved black arrows) as
well as slight subluxation of the lens (dashed black arrow).
In comparison with CT, MR imaging requires a higher sensitivity for pathologic processes, such
larger commitment in terms of time, cost, and pa- as inflammatory and neoplastic lesions (Figs. 9–13).
tient cooperation but continues to play a growing, The anatomy of the head and neck presents
indispensable role in head and neck imaging. Pa- specific challenges for MR imaging evaluation, as
tients who are either very young, distressed, or the inherent bony anatomy and air interfaces of
presenting with altered levels of consciousness the head and neck create artifacts related to mag-
may also require sedation or even general anes- netic field inhomogeneity. Motion from breathing,
thesia in order to successfully complete an MR im- swallowing, and vascular pulsatility can further
aging examination. These patients require close degrade image quality. Artifact from physiologic
monitoring by dedicated personnel, so this should motion can often be minimized by careful satura-
be kept in mind when planning a potential scan. tion band placement, cardiac gating, switching
Before the examination, rigorous screening for the frequency/phase encoding axes, and effective
metallic foreign bodies or implanted electronic coaching for breath-holds and cessation of swal-
medical devices should be performed to ensure lowing. Further innovations built around faster
safe, efficacious scanning, so as to prevent injury pulse sequences, higher temporal resolution,
to patients or damage to sensitive indwelling hard- lower specific absorption rates, and precision
ware. At high-magnetic-field strength (3.0 T) MR saturation of fat signal may improve visualization
imaging provides a higher signal-to-noise ratio of complex anatomic structures.
and improved delineation of soft tissue structures.
Higher-field MR imaging may, thus, provide a Generally speaking, all of the imaging protocols
rely on multiplanar images centered over a small
220 Brucker & Gentry
Fig. 7. Bilateral Le Fort I, II and III fractures with posttraumatic retrobulbar mass effect and posterior globe tent-
ing: Axial (A), oblique sagittal (B), and 3-dimensional (3D) (C) CT scans reveal extensive bilateral Le Fort I to III
facial fractures. There is evidence of a small amount of intravitreal (black arrowhead) and subretinal (black arrow)
hemorrhage as well as an abnormally elongated right globe. There is flattening (tenting) of the posterior aspect
of the globe (white arrows) indicating retrobulbar mass effect. The oblique sagittal and 3D CT images reveal up-
ward displacement of the orbital floor (curved black arrows) decreasing the volume of the orbit resulting in the
mass effect.
FOV with a large matrix. For CT, the authors ac- to successful head-and-neck imaging is to under-
quires 0.65-mm axial images and performs thin stand the problem at hand and the clinician’s
( 2 mm) 2-dimensional (2D) reconstructions in request. Such comprehension will not infrequently
the sagittal and coronal planes with both soft tis- require personally reviewing the patient’s medical
sue and bone reconstruction algorithms. MR im- record, familiarizing oneself with their past medical
aging protocols are inherently more complicated history and presenting issues, and having a brief
than their CT counterparts but always include pre- discussion with the ordering provider.
contrast triplanar T1-weighted images, 2-planar
T2-weighted images, and propeller-based fast Teaching point: Successful prescription of a
spin echo diffusion-weighted imaging. Triplanar head and neck imaging protocol is always pre-
postcontrast T1-weighted images are then ac- ceded by a review of the patients’ medical
quired in the same locations as the precontrast information.
T1-weighted images. The variation between indi-
vidual protocols is driven by the area of anatomic EMERGENCIES OF THE ORBIT
coverage that is needed and the clinical indication.
In practice, protocols often need to be tailored to a Very few things inspire a trip to the emergency
specific patient’s situation. Therefore, the first step department as effectively as something unpleas-
ant happening to your eye, which frequently
Imaging of Head and Neck Emergencies 221
Fig. 8. Ethmoid-maxillary sinusitis, subperiosteal orbital abscess, and epidural abscess: Coronal (A), axial (B, C),
and sagittal (D) CT images reveal maxillary and ethmoid sinus opacification (star) consistent with acute sinusitis.
There is a hypodense subperiosteal abscess (white open arrows) with peripheral enhancement of the displaced
orbital periosteum. Early postseptal orbital cellulitis is indicated by edema of the retro-orbital fat and medial
rectus muscle (dashed white arrow). One should always carefully look at the intracranial contents in anyone
with sinusitis in order to detect intracranial complications, such as this gas-forming epidural abscess (white
arrows).
occurs in the context of blunt or penetrating accompanying complaint of ocular discomfort or
craniofacial trauma. Although a great deal of emer- vision impairment. Generally speaking, pene-
gent orbital imaging is performed as a part of the trating orbital injury usually implies 2 types of major
workup for facial trauma, the authors limits his consequences that require intervention: (1) direct
discussion to intraorbital emergencies that are injury to the intraorbital soft tissue structures (see
not secondary to acute traumatic compromise of Fig. 2) and (2) retention of an intraorbital foreign
the bony orbit. Therefore, the authors focuses on body (see Figs. 3 and 4). During situations in which
penetrating intraorbital injury (see Figs. 2–4), an obvious foreign body is protruding from the
orbital infections (see Figs. 8–11), and acute orbit (see Fig. 2), attempts at removal should not
noninfectious inflammatory conditions of the be performed in the field for risk of exacerbating
neuro-ocular complex (see Figs. 12 and 13). the injury and inducing intraorbital hematoma.
Orbital penetration should be suspected in any
Penetrating Orbital Injury patient with a history of high-velocity trauma to
the face and orbits. This trauma includes shrap-
It is usually not difficult for the clinician to deter- nel from explosions, wood shop mishaps, tree
mine if there has been a penetrating intraorbital branches snapping back into one’s face, poorly
event, as there is often obvious disruption to the caught bridal bouquets, and other tragedies of
external soft tissues on examination, with an daily life.
222 Brucker & Gentry
Fig. 9. Subperiosteal orbital abscess: Coronal CT scan (A) as well as oblique sagittal T1-weighted (B), coronal
T2-weighted (C), and coronal postcontrast fat-suppressed T1-weighted (D) MR images demonstrate a large super-
omedial subperiosteal orbital abscess (asterisk) in this patient who presented with a 2-week history of progressive
proptosis and visual loss. The lamina papyracea (black arrow) is seen to be eroded on the CT scan. The abscess is
lenticular, centrally nonenhancing, and peripherally enhancing and causes marked mass effect on the superome-
dial group of extraocular muscles. The superior rectus, levator palpebrae superioris, medial rectus, and superior
oblique muscles (white arrowheads) are inferolaterally displaced. Postseptal orbital cellulitis is manifested by
dirty fat on the T2-weighted image, strandlike enhancement of orbital fascia, and poor definition and enhance-
ment of the involved muscles (white arrowheads). Pachymeningeal enhancement (curved white open arrows) is
present indicating early intracranial spread of infection.
One of the strongest imaging signs of a pene- should raise suspicion of a penetrating injury.
trating intraorbital injury is the presence of intraor- Furthermore, any accumulation of intraorbital air
bital air, particularly if it is seen within the that is large enough to create significant mass
extraocular musculature (see Fig. 2) or within the effect should be separately discussed and sug-
globe itself. In many cases, however, a penetrating gested as a possible penetrating event. Excessive
object will take the path of least resistance and in trapped retrobulbar air can result in a tension
doing so glance off of the firmest intraorbital struc- pneumo-orbit in which there is proptosis, stretch-
tures, such as the sclera and tendon insertions, ing of the optic nerve, and tenting of the posterior
and the air will preferentially accumulate within globe. If overlooked, possible long-term sequelae
the intraconal and extraconal fat. In these situa- of tension pneumo-orbit include optic nerve
tions, any collection of intraorbital air that is either ischemia from compression of the ophthalmic ar-
very focal in distribution, linear in configuration, tery or veins, optic nerve injury secondary to
associated with intraorbital hematoma (see mass effect, retinal detachment, and blindness.1,2
Figs. 4, 6 and 7) or foreign body (see Figs. 3 and
4), or seen in the absence of orbital wall fracture Other imaging features of orbital injury may be
more obvious, such as completely detached
Imaging of Head and Neck Emergencies 223
Fig. 10. Orbitorhinocerebral fungal infection (Aspergillus): Coronal T1-weighted (A), axial T2-weighted (B), as
well as axial (C, D), coronal (E) postcontrast fat-suppressed T1-weighted, and contrast-enhanced MR angiographic
(F) images in this immunocompromised patient demonstrate extensive infection of the sinuses, right orbit, and
brain (frontal and temporal lobes). Postseptal orbital cellulitis is revealed by enlargement and peripheral irregu-
larity of several extraocular muscles (white arrows). The fungal nature of the infection can be suspected by the T2
hypointense areas of inflammation in the sphenoid sinus and pterygopalatine fossa (curved white arrows). Post-
contrast images reveal areas of abnormal enhancement (black arrowheads) within the orbit indicating orbital
cellulitis as well as areas of rindlike enhancement (white arrowheads) within the frontal and temporal lobes
of the brain consistent with cerebritis. Importantly, however, there are extensive central areas of nonenhance-
ment (open white arrows) in the orbit and brain that indicate infected nonperfused necrotic tissue. These areas
of necrosis must be surgically removed because the lack of perfusion means antibiotics will not reach these areas.
Cavernous sinus thrombophlebitis is revealed by a lack of normal enhancement within the cavernous sinus on MR
imaging (curved black arrow) and MR angiography (curved open white arrow).
extraocular muscles, lens dislocation or disruption extraconal fat within the anterior superolateral
(see Figs. 3 and 4), severed optic nerve, and orbit. The lacrimal glands should be symmetric
deflated globe (see Figs. 4 and 6). Several subtle as well as homogeneous in CT attenuation and
injuries may be missed unless one specifically enhancement pattern. Focal fluid collections or
looks for them. For example, the medial canthus linear hypoenhancing areas within the lacrimal
should be inspected for disruption of the medial gland are concerning for laceration. Contrast-
canthal ligament or avulsion of the bony attach- enhancement may also facilitate the detection of
ment of this ligament (see Fig. 5), injury to the na- partial-thickness lacerations through the extraocu-
solacrimal drainage system (see Fig. 5), and lar muscle bellies, which may manifest as linear
hyphema (see Figs. 4 and 6). Medial canthal liga- hypoenhancement extending along the path of
ment avulsion may manifest as either focal hema- injury or irregular margins of the muscle with
toma in that location or lateral subluxation of the stranding of the adjacent fat. The presence of a
globe. Injuries to these structures usually require radiopaque foreign body in any of these locations
surgical repair. Similarly, injury to the lateral suggests a penetrating injury until proven
canthal region should not be overlooked. Inspec- otherwise.
tion of this area should also include evaluation of
the lacrimal gland, which is located within the As mentioned earlier, the presence of intraorbi-
tal air can be associated with a retained foreign
224 Brucker & Gentry
Fig. 11. Subperiosteal orbital abscess, orbital cellulitis, meningitis, subdural empyema: Axial T1-weighted (A),
axial T2-weighted (B), as well as axial (C) and coronal (D) postcontrast fat-suppressed T1-weighted images demon-
strate a subperiosteal orbital abscess (star) in this patient with progressive headache, retro-orbital pain, and loss
of vision. Postseptal orbital cellulitis is revealed by edema and enhancement of the postseptal orbital fat. Orbital
myositis is also present with edema, enlargement, peripheral irregularity, and enhancement of the medial rectus
muscle (open white arrows). The coronal image reveals extensive intracranial spread of infection with abnormal
enhancement of the leptomeninges (curved open white arrows), subdural empyema (white arrow) and frontal
lobe cerebritis (dashed white arrow).
body, and the detection of one should prompt a radiography compared with other types of foreign
search for the other. Most intraorbital foreign bodies. In order to increase sensitivity for tiny
bodies tend to be made of metal or glass, and metallic fragments, it is recommended that one
these materials are characteristically hyperdense also review images reconstructed with a bone al-
on CT (see Figs. 3 and 4). MR obviously should gorithm. It is common for radiopaque foreign
be avoided if a ferromagnetic foreign body is sus- bodies to collect along the folds of the eyelids
pected. The CT attenuation of glass is variable and and between eyelashes, representing cutaneous
ultimately depends on its mineral composition and periorbital debris instead of a true retained radi-
manufacturing process, ranging anywhere from opaque foreign body. In contradistinction, any pre-
several thousand Hounsfield units (HU) to minus septal densities abutting the surface of the cornea
200 HU.3 There is less variability on CT for metallic and sclera or lying deep to the eyelid tarsus should
fragments because most metal will near com- raise suspicion of a foreign body either located on
pletely attenuate the x-ray beam. Metallic shav- or below the conjunctival layer. The diagnosis is
ings and splinters are often extremely small but clinched by ophthalmologic examination with fluo-
will demonstrate a high level of attenuation that rescein. In addition to persistent eye irritation, re-
is out of proportion to their size, accounting for tained inorganic foreign bodies can lead to the
their ability to be reliably detected on plain film presence of intraorbital rust deposits as well as
Imaging of Head and Neck Emergencies 225
Fig. 12. Optic neuritis (neurosarcoidosis): Axial T2-weighted (A), coronal T2-weighted (B), as well as axial (C) and
coronal (D) postcontrast fat-suppressed T1-weighted images were obtained in this patient with a 2-week history
of retro-orbital pain, loss of vision, and left optic nerve papillitis. The T2-weighted images reveal marked enlarge-
ment and edema of the left optic nerve (white arrows) as well as marked papilledema (black arrowhead). There is
a fuzzy appearance of the optic nerve on the coronal T2-weighted image indicating coexistent optic perineuritis.
Contrast-enhanced images reveal extensive enhancement (curved open white arrows) of the optic nerve, optic
sheath, and optic nerve head (white arrowhead). The presence of orbital pain, visual loss, and combination of
optic neuritis and perineuritis suggest an inflammatory optic neuritis, such as neurosarcoidosis.
reactive aggregations of inflammatory cells. Re- often redolent with bacteria and fungi and can ulti-
moval of these foreign bodies is sometimes mately lead to serious intraorbital infections.
achieved by microreaming of the surrounding
affected tissue.4 Orbital Cellulitis
Although often heralding the presence of a Many of the orbital infections leading to emergent
foreign body in some case, intraorbital air may imaging are limited to the superficial periorbital
actually impede the identification of foreign bodies soft tissues that are relatively confined to the
composed of wood or certain low-weight plastics. orbital septum, henceforth distinguished as pre-
Retained wood products, whether they are fresh or septal cellulitis. It can represent local progression
old, are often radiolucent on CT as well as hypoin- of a preceding skin or eyelid condition, such as
tense on most MR sequences, making it difficult to blepharitis, furuncles, or other adjacent cutaneous
distinguish from air.5 Although wood often ap- infection. Consistent with its superficial cutaneous
proaches air attenuation on CT, inspecting the roots, Streptococcus, Staphylococcus, Pneumo-
orbits with a dedicated lung window may help coccus, and Pseudomonas are among the most
aid in detection and discrimination of these mate- common infecting organisms. Preseptal cellulitis
rials. The presence of an intraorbital wood product is usually unilateral and presents as marked
has added significance in that organic material is
226 Brucker & Gentry
Fig. 13. Idiopathic orbital inflammatory disease: Oblique sagittal T1-weighted (A), axial T2-weighted (B), as well
as axial (C) and coronal (D) postcontrast fat-suppressed T1-weighted images were obtained in this patient with
painful ophthalmoplegia and rapid decrease of vision. There is an extensive ill-defined soft tissue mass (white
arrows) extending along the superior rectus and levator palpebrae superioris muscle as far anteriorly as the upper
eyelid. There is enlargement, edema, and abnormal enhancement of the medial rectus muscle (curved white ar-
rows) as well as the superior rectus (curved white open arrow) and superior oblique (dashed white arrow) mus-
cles. Optic perineuritis is manifested by abnormal enhancement of the optic sheath (white arrowheads). The
ophthalmoplegia is likely caused by involvement of the cranial nerves 3, 4, and 6 as they traverse the inflamma-
tory mass (open white arrows) in the superior orbital fissure and cavernous sinus.
induration, tenderness, and erythema of the eyelid, conjunctivitis is often either allergic or viral in origin
sometimes seen in association with a stye. instead of bacterial; the presentation is, therefore,
Conversely, decreased visual acuity, restricted ex- frequently bilateral.4,6–8
traocular movements, exophthalmos, and marked
injection and bogginess of the conjunctiva (che- Radiology does not typically play a role in the
mosis) are not expected in preseptal cellulitis and diagnosis of acute conjunctivitis unless it is to
should instead raise concern for an acute process exclude the additional presence of preseptal or
occurring within the postseptal orbit. That being postseptal cellulitis. In preseptal cellulitis, the
said, it is possible for chemosis to present in radiologic findings will closely follow the clinical
more advanced cases of preseptal cellulitis presentation, with marked thickening of the eyelid
because of local reactive changes. Chemosis sec- and adjacent superficial soft tissues as well as
ondary to conjunctivitis can also be confused with requisite sparing of the postseptal soft tissues. In
orbital cellulitis on clinical evaluation, although the severe cases, it may be possible to discern small
inflammatory findings are usually limited to the fluid collections and microabscesses forming
conjunctival membrane without other discrete within the eyelid, which further secures the diag-
signs to suggest postseptal cellulitis. Furthermore, nosis. When evaluating the orbits, especially if
preseptal cellulitis is suspected, close attention
Imaging of Head and Neck Emergencies 227
should be paid to the paranasal sinuses and naso- postseptal cellulitis can have tremendous overlap,
lacrimal complex because infection and obstruc- including extraocular muscle restriction (vs palsy),
tion of these structures may incite edema within proptosis, papilledema, headache, fever, and peri-
the preseptal soft tissues that masquerades as orbital swelling. Additional palsies involving the V1
true cellulitis. It can be very difficult to distinguish or V2 branches of the trigeminal nerve, lateral
early preseptal cellulitis from reactive preseptal bowing of the cavernous sinus wall, or hypoen-
edema. In fact, both entities may be present at hancement of the cavernous sinuses (see Figs. 8
the same time, although unilateral periorbital dis- and 10) are, therefore, ominous findings.
ease in the setting of bilateral sinusitis may be a
clue of a distinct preseptal infection.6–9 Inflamma- As with preseptal cellulitis, the adjacent para-
tion and congestion of the preseptal soft tissues nasal sinuses should be part of the search pattern
can also be secondary to an underlying postseptal when evaluating postseptal cellulitis. Most post-
infection. septal cellulitis cases start as bacterial ethmoid
sinusitis (see Figs. 8–11) that has gained access
The key imaging feature of postseptal cellulitis is to the orbits via foramina and tiny osseous fenes-
stranding of the intraorbital fat (see Fig. 9), which trations. For this same reason, the formation of a
represents a combination of edema, vascular subperiosteal abscess between the periorbita
congestion, increased microvascular permeability, and bony orbit often accompanies the diagnosis
and inflammatory infiltrates. As the infection pro- of postseptal cellulitis. This postseptal cellulitis
gresses, the stranding may become more coales- typically appears as lenticular fluid collections
cent and exhibit increasing intraorbital mass (see Figs. 8–11) extending along the lamina papy-
effect. These inflammatory changes may cause racea or medial orbital roof, with extrinsic mass ef-
stretching of the optic nerve and tenting of the fect exerted on the medial conal and extraconal
posterior globe, thereby indicating an impending structures. Vision and ocular motility may be
threat to the patients’ vision. compromised as the subperiosteal abscess ex-
tends back to the orbital apex with compromise
Other critical developments in advanced post- of the optic nerve and cranial nerves III to
septal cellulitis include the development of sub- VI, respectively. In advanced cases, abscess for-
periosteal abscess (see Figs. 8–11), extraocular mation can even be directed intracranially (see
muscle myositis (see Figs. 8–11), formation of Figs. 8 and 10).6,8
an intraorbital abscess, and orbital venous throm-
bophlebitis. Detection of muscular and vascular Teaching point: Identification of intraorbital dis-
complications usually requires a contrast- ease should prompt the evaluation of the paranasal
enhanced CT or MR imaging examination, as sinuses for a potential underlying cause.
opposed to the detection of intraorbital fat strand-
ing, which is readily seen on noncontrast examina- Noninfectious Orbital Inflammation
tions. These entities will also necessitate more
aggressive management and surveillance. Intraor- In the absence of intraorbital abscess or other
bital abscesses should appear on CT as isodense clear evidence of orbital infection, inflammatory
to hypodense fluid collections with rim enhance- changes to the postseptal soft tissues are not
ment and perilesional edema. On MR, dedicated necessarily specific on imaging.10 Noninfectious
T2-weighted images with fat saturation may better conditions (see Figs. 12 and 13) may present
delineate tiny fluid pockets scattered throughout with acute loss of vision, orbital pain, or impair-
the intraorbital soft tissues. Diffusion-weighted im- ment of ocular motility and require urgent evalua-
aging also aids in the detection of intraorbital ab- tion as to the cause of the symptoms. Stranding
scesses because these lesions may exhibit of the intraorbital fat, proptosis, and periorbital
restricted diffusion, reflecting the viscous contents edema is encountered across wide ranges of
of the abscess cavity. This is particularly useful in noninfectious conditions; the diagnosis cannot al-
situations in which contrast cannot be adminis- ways be made on an imaging basis alone. Imag-
tered. MR imaging can also aid in the diagnosis ing, however, does play a role in identifying the
of orbital thrombophlebitis, which may demon- presence of an inflammatory process and helping
strate as enlarged, T1-hyperintense veins seen determine which of the intraorbital structures are
against a background of extensive intraorbital involved.
edema. Of note, orbital thrombophlebitis can
extend intracranially through valveless veins and For example, inflammatory changes that are pri-
result in thrombosis of the cavernous sinus (see marily localized to the extraocular muscles and ten-
Fig. 10). This severe complication is associated dons (see Fig. 13) usually indicate a diagnosis
with high morbidity and mortality. The clinical pre- of orbital myositis. These structures will be en-
sentations of cavernous sinus thrombosis and larged, hyperenhancing, and possess shaggy bor-
ders with adjacent fat stranding. Alternatively,
228 Brucker & Gentry
inflammatory changes might be limited to the ante- clue is not always available. The specific imaging
rior and posteriors margins of the globe (episcleri- features of optic neuritis are more readily apparent
tis), optic nerve head (papillitis), optic sheath on MR, presenting as fusiform enlargement, T2 hy-
(perineuritis), Tenon’s capsule (sclerotenonitis), perintensity, and hyperenhancement of the
various components of the uveal tract (uveitis), op- affected nerve. Although this presentation may
tic nerve sheath (perineuritis), optic nerve (optic represent acute optic neuritis in isolation, dedi-
neuritis), lacrimal gland (dacryoadenitis), and so cated imaging of the brain and spinal cord is rec-
forth. Inflammatory changes of the nasolacrimal ommended to evaluate for an underlying
complex (dacryocystitis) should trigger close in- diagnosis of multiple sclerosis or neuromyelitis op-
spection of the sinonasal cavity in order to exclude tica or other inflammatory and granulomatous
a possible obstructing lesion or infection.6,11 conditions affecting the central nervous system
(such as sarcoidosis).6,11,13
Intraorbital inflammatory changes may also
encompass a larger set of structures that are EMERGENCIES OF THE SINONASAL CAVITY
related by a shared anatomic region, such as the
entire anterior orbit (anterior orbital pseudotumor) Acute complaints centered on the nasal cavity
and within the orbital apex (orbital apex inflamma- and paranasal sinuses are frequently encountered
tory syndrome). All of these orbital inflammatory in the primary and emergent care settings, largely
conditions may be considered part of a larger set in thanks to the widespread existence of inflam-
of inflammatory diseases, collectively referred to matory sinus disease, environmental allergies,
as idiopathic orbital inflammatory syndrome, or and the common cold. Although unpleasant in
sometimes orbital pseudotumor given their ten- their own right, they rarely require urgent imaging.
dency to cause mass effect and non-neoplastic Urgent imaging of the sinuses may be necessary,
masslike expansion of the native intraorbital struc- however, when patients are immunocompro-
tures.11,12 This inflammation is often idiopathic in mised, diabetic, or if there is clinical suspicion of
that the inciting cause cannot be ascertained. orbital or intracranial extension of disease. In
When one encounters any one of these disease these situations, a more sinister process that
entities, one must also consider several systemic could pose serious endangerment to patients
conditions, including cytoplasmic antineutrophil must be excluded. Of these entities, the authors
cytoplasmic antibody (c-ANCA)–positive granulo- emphasizes complications of acute bacterial
matosis with polyangiitis (formerly Wegener gra- sinusitis, acute invasive fungal sinusitis, and fulmi-
nulomatosis), rheumatoid arthritis, Sjo¨ gren nant epistaxis.
syndrome, systemic lupus erythematosus, other
autoimmune disorders, and sarcoidosis. Lym- Acute Bacterial Sinusitis
phoma, pseudolymphoma, and leukemia exist as
both potential causes of orbital inflammatory syn- Most acute rhinosinusitis cases are viral in cause
drome as well as distinct mimics of the disease. and, therefore, exhibit a self-limiting course, as-
Any of these conditions may manifest as a hyper- suming the absence of comorbid factors. However,
cellular, infiltrative intraorbital soft tissue mass with persistent or worsening sinonasal symptoms, such
characteristic enhancement, restricted diffusion, as high fever, mucopurulent discharge, orbital pain,
and relative T2-hypointensity. Perusal of the pa- and periorbital edema, are concerning for more
tients’ medical records is highly encouraged at serious bacterial infections in immunocompetent
this point. patients. In particular, unilateral symptoms or
symptoms persistent beyond 10 days from onset
Out of the abovementioned idiopathic inflamma- are worrisome for a bacterial sinusitis, possibly
tory conditions of the orbit, perineuritis (see superimposed on a preceding viral infection.14–16
Fig. 12) of the optic nerve sheath may represent
another potential diagnostic pitfall, occasionally Several conditions usually need to be met in
being confused with optic neuritis. Clinically, these order for an acute bacterial sinusitis to develop;
two diseases may each present as acute-onset in- impairment of normal sinus drainage provides an
traorbital pain and vision loss, although only optic opportunity for bacteria to establish themselves
neuritis represents acute inflammation of the optic within the sinus cavity and is usually the result of
nerve fibers instead of the surrounding dural multiple factors, including (1) obstructed sinus
sheath. On CT, both disease entities may demon- drainage pathways and ostia, (2) abnormal sino-
strate apparent enlargement of the optic nerve- nasal mucosa, (3) decreased mucociliary clear-
sheath complex with perineural fat stranding. In ance, and (4) abnormal consistency of sinus
these cases, additional involvement of the Tenon’s secretions. Impaired immune function is an addi-
space may help make the diagnosis of perineuritis tional risk factor for both bacterial and fungal sinus
over optic neuritis, although this differentiating infections.
Imaging of Head and Neck Emergencies 229
Most bacteria are introduced to the sinus cav- Acute Invasive Fungal Sinusitis
ities via the nasal mucosa and are caused by
Staphylococcus, Haemophilus, Streptococcus, There are various forms that fungal infections of
and Moraxella species. Additionally, several acute the nasal cavity and paranasal sinuses can take;
bacterial sinusitis cases are dental in origin (odon- but the most aggressive type, and the one carrying
togenic) and can be caused by anaerobic infec- the worst prognosis, is acute invasive (fulminant)
tions. Therefore, the presence of sinonasal fungal sinusitis. This infection is almost exclusively
disease should trigger a close examination of the encountered in patients with impaired immune
maxillary dentition, and vice versa.15 systems (AIDS, organ transplantation, systemic
neoplasms, chemotherapy recipients) or other
Inflammatory changes of the paranasal sinuses, significant systemic metabolic disease (poorly
regardless of their cause, are usually accom- controlled diabetes, renal failure, cirrhosis), so be-
panied by enhancement and thickening of the mu- ing aware of these major preexisting medical prob-
cosa, with varying degrees of submucosal edema lems beforehand is an important step toward
and intraluminal secretions. The severity and making the diagnosis.
pattern of these findings are not entirely specific
to acute bacterial infection and can be observed In the immunocompromised patient population,
in both chronic and nonbacterial disease. Air- fungal sinonasal infection is usually secondary to
fluid levels are lacking in complete specificity but Aspergillus species (see Fig. 10), which are ubiqui-
are regarded as an important sign for identifying tous in the environment and gain access to the
acute bacterial sinusitis.15 paranasal sinuses by colonizing the nasal mucosa.
Fungi belonging to the Zygomycetes class
Incompletely treated or otherwise unmitigated (Rhizopus, Mucor) thrive in glucose-rich environ-
acute bacterial sinusitis has the potential to extend ments. This fact coincides with the general
beyond its original boundaries, resulting in various consensus that severely diabetic patients (for
complications, usually in the form of subperiosteal example, those presenting in acute ketoacidosis)
abscesses (see Figs. 8–11). These complications are the prototypical target population, although
may present themselves rather suddenly after a immunocompromised patients are also certainly
protracted course of sinonasal symptoms if the at high risk. Regardless of the specific fungal spe-
involved sinus cavity is subjected to a rapid in- cies at work or the clinical background, acute
crease in sinonasal pressure, such as with forceful fulminant fungal sinusitis is consistent in its char-
nose blowing. For example, in the setting of acute acteristic rapid progression and aggressive inva-
ethmoidal sinusitis, the infection can extend later- sion through the sinus walls and extension along
ally through the lamina papyracea, producing a blood vessels into adjacent structures (see
subperiosteal abscess along the medial and super- Fig. 10). Intraorbital or intracranial spread of
omedial walls of the orbit. Frontal sinusitis has the disease can occur as quickly as within 24 to
option of extending through either the outer or inner 72 hours; severe complications include the devel-
cortex of the frontal bone. Permeation through the opment of subperiosteal abscess, empyema,
outer table can result in abscess formation in the meningitis, cerebritis, cerebral infarction, dural
superficial soft tissues of the scalp, which will pre- and cavernous sinus thrombosis, and often death.
sent clinically as a fluctuant inflammatory mass Despite rapid intervention with surgical debride-
along the forehead (Pott puffy tumor). With further ment and high-dose intravenous antifungal
extension of the myofasciitis, there will be involve- agents, the overall mortality rate remains
ment of the frontalis muscle. Extension of sinusitis extremely high.14,15,17
through the inner table of the frontal sinus can result
in formation of epidural or subdural empyema, On imaging, acute invasive fungal sinusitis can
meningitis, or frontal lobe encephalitis. Frontal share features with other forms of sinusitis,
sinusitis can extend through a pneumatized hori- including T2 hyperintense mucosa that is thickened
zontal plate of the frontal bone directly into the orbit. and enhancing; but fungal infection should be sus-
Complications from acute sphenoid sinusitis can pected in the presence of debris that is T2 hypoin-
manifest as osteomyelitis of the skull base, tense and restricts diffusion. Early invasive fungal
cavernous sinus thrombophlebitis (see Fig. 10), or sinusitis can be primarily a soft tissue infection.
abscess formation along the retroclival and para- Later on, erosive changes to the adjacent sinus
cavernous regions.14,15 wall with transosseous spread are more obvious
imaging clues for invasive fungal sinusitis. These
Teaching point: Identification of sinonasal dis- changes, however, are not required to make the
ease should prompt inspection of the dentition diagnosis but may only be seen in advanced stages
just as identification of intraorbital disease should of the disease. Early invasion is often conducted
prompt inspection of the sinuses (the inverse is along small traversing vessels of the skull base,
also true).
230 Brucker & Gentry
allowing unencumbered spread into the intracra- In the region of the anterior nasal cavity, 2
nial space via natural foramina.18 It is quite impor- important anastomotic sites should be consid-
tant to look for areas of hypoenhancement on ered. One is between the dorsal nasal artery (a ter-
imaging in these patients. These areas usually indi- minal branch of the ophthalmic artery) and angular
cate necrotic nonperfused tissue (see Fig. 10) that artery (a terminal branch of the facial artery) at the
must be surgically debrided because antibiotics level of the medial canthus, sometimes referred to
will not be able to penetrate these areas. as the orbital point. Another is between the supe-
rior labial artery (another terminal branch of the
Teaching point: Osseous destruction can be a facial artery) and the anterior ethmoidal artery, at
late sign of acute invasive fungal sinusitis. Any si- the level of the columella.21
nonasal process associated with T2 hypointensity
and restricted diffusion should raise concern for In the posterior nasal cavity, anastomotic con-
an aggressive disease process, despite apparent nections exist between the branches of the sphe-
intact bony architecture. nopalatine artery and ethmoidal branches of the
ophthalmic artery as well as with the greater pala-
Epistaxis: Hemoptysis tine artery. The presence and arrangement of
these connections tend to be highly variable be-
The authors admits that nosebleeds are usually a tween individual patients, so they are not des-
self-limited condition bearing little to no significant cribed here.21
clinical consequence. Most cases are associated
with irritation or injury to a rich vascular plexus The branches of the anterior and posterior
(Kiesselbach plexus) within the anterior nasal vascular supply intersect at a rich vascular plexus
septum and easily treated with transient pressure. along the anterior nasal septum, also known as
The eruption of blood from the nasal cavity is often Kiesselbach plexus or Little’s area. This site is
a nonspecific finding but can, on occasion, indi- common for epistaxis, particularly in children,
cate the presence of a serious underlying condi- and is often easily treated with tamponade.
tion. In particular, high volume and recurrent Treatment of posterior epistaxis can also be at-
epistaxis is more likely to be caused by several tempted with nasal packing but may require
worrisome medical conditions, including benign more invasive interventions, such as clipping or
and malignant neoplasms, accidental and iatro- embolization.22–24
genic trauma, granulomatous disease, vascular
malformations (both acquired and hereditary), Hemoptysis (expectoration of blood, blood-
and acute sinusitis (bacterial or fungal). These con- stained sputum) usually has its source lower in
ditions can be associated with high morbidity and the airway (pharynx, larynx, trachea, bronchi,
mortality, so effective and appropriate treatment lungs) and is discussed more thoroughly later in
relies on a timely diagnosis.19,20 the article (Fig. 14).
In theory, epistaxis can be induced by any pro- EMERGENCIES OF THE TEMPORAL BONE
cess that leads to injury or derangement of the
normal vasculature. Therefore, the differential for When considering the temporal bone, many peo-
intranasal bleeding is broad. Generally speaking, ple think primarily about the part of our anatomy
epistaxis can be categorized by location: anterior that is chiefly concerned with hearing, whereas,
versus posterior, lateral versus septal, and internal in all fairness, it interfaces with a diverse set of
versus external carotid supply. equally important and functionally disparate struc-
tures. Therefore, evaluation of the temporal bone
The nasal cavity receives blood supply from should include inspection of more than the ossi-
both the internal carotid (via branches of the cles, labyrinth, and internal/external auditory
ophthalmic artery) and external carotid arteries canals. Among other things, the petrous internal
(via branches of the sphenopalatine and facial ar- carotid canal, sigmoid sinus, jugular foramen,
teries). The territories of these arterial branches facial nerve, Meckel cave, and cranial fossae are
demonstrate a high degree of overlap, which all potential sites of collateral damage in temporal
carries 2 important consequences: (1) It provides bone disease.
a robust network of collateral flow to preserve
the viability of delicate soft tissues throughout Necrotizing (Malignant) Otitis Externa
the nasal cavity. (2) It allows for anastomotic
routes between the internal and external arterial Not to be confused with the more frequently
circulation. Both scenarios can complicate the encountered swimmer’s ear, malignant otitis ex-
management of epistaxis, which may be refractory terna is a severe necrotizing infection of the
in some cases or associated with unintentional external ear and subadjacent skull base. It is typi-
embolization of the retina or brain in others. cally caused by Pseudomonas aeruginosa and is
seen in patients who are elderly, diabetic, and/or
Imaging of Head and Neck Emergencies 231
Fig. 14. Hemoptysis, carotid blowout, advanced tonsillar squamous cell carcinoma: Lateral (A) and anteroposte-
rior (B) carotid angiogram images in a patient presenting with hemoptysis. The patient had a history of recurrent
squamous cell carcinoma of the tonsil that was encasing the carotid bifurcation on CT scans (not shown). The
angiogram demonstrates narrowing and irregularity of a long segment of the internal carotid artery (arrow-
heads) at the site of carotid encasement. Two focal areas of external carotid artery ulceration (arrows) are present
at the sites of the carotid blowout.
immunocompromised. Clinically, these patients Also, as seen in acute bacterial sinusitis, acute
present with severe otalgia, purulent otorrhea, otomastoiditis can be further complicated by
and inflammatory changes tracking along the extension beyond the confines of the mastoid pro-
external ear and external auditory canal. Radiolog- cess and tympanic space. Externally directed
ically, one may expect to discover an erosive soft extension in the overlying soft tissues may mani-
tissue mass in this location, with blatant violation fest as subperiosteal abscess formation along
of the underlying osseous boundaries. Invasion the mastoid process surrounded by periauricular
of the temporomandibular joint, parotid gland cellulitis. A specific form of subperiosteal abscess
mastoid process, middle cranial fossae, and cra- (Bezold abscess) occurs when the abscess arises
nial nerves can be features of this disease, so it along the inferior tip of the mastoid process,
is not hard to imagine why this particular process around the digastric groove, and extends along
has an associated high mortality rate. the insertion of the sternocleidomastoid muscle
(Fig. 15). This abscess is most readily identified
Acute Otomastoiditis as a rim-enhancing fluid collection on coronal
plane imaging.14
Acute bacterial infections of the tympanic cavity
and mastoid air cells share several features with Medially directed extension of the infectious
acute bacterial infections of the paranasal sinuses. process may result in extension through the sig-
That is, most infections are usually the result of moid plate into the subdural or epidural spaces
either Haemophilus or Streptococcus species in of the posterior fossa. As a consequence of this
the setting of impaired drainage of the mastoid location, the infection may cause sigmoid sinus
air cells and tympanic spaces. This setup is most thrombophlebitis and impairment of sigmoid and
notably encountered in younger children, given transverse sinus venous drainage (Fig. 16). This
the more horizontal configuration of the eustachian impairment can, in turn, lead to increased intracra-
tubes in early age, although sterile mastoid and nial pressure and venous infarctions, often in the
tympanic effusions are frequently encountered distribution of the vein of Labbe´ . These patients
and often carry no acute clinical significance. may have additional symptoms of photophobia,
However, opacification of the air spaces in a pa- retro-orbital headache, dizziness, and nausea.
tient with fever, otalgia, middle ear effusion, and Dedicated imaging of the dural venous sinuses
postauricular headache are classic signs of acute with CT venography (CTV) or MR venography
otomastoiditis. As with acute bacterial sinusitis, (MRV) may be indicated. On CTV, a hyperdense
the presence of air-fluid levels in the mastoid air appearance of the dural sinuses on precontrast
cells is very suggestive of acute otomastoiditis. imaging, or a hypoenhancing filling defect on post-
contrast imaging, are useful clues in making the
232
Fig. 15. Acute otomastoiditis, subperiosteal (Bezold) abscess, dural venous thrombophlebitis: A 4-year-old unre-
sponsive child with rapid development of a mass extending along the lateral aspect of the right temporal bone
into the upper aspect of the sternocleidomastoid muscle. Contrast-enhanced temporal bone CT scans (A, B)
demonstrate opacification of the tympanic (dashed white arrow) and mastoid (open white arrow) cavities but
no obvious cortical bone erosion. There is a large peripherally enhancing subperiosteal abscess (black arrow)
lateral to the mastoid and squamous portions of the temporal bone. There is thrombosis of the sigmoid sinus
(white arrow) and signs of meningitis with abnormal enhancement of the tentorium (curved open white arrows).
Fig. 16. Acute otomastoiditis, epidural abscess, dural venous thrombophlebitis: A 3-year-old boy who presented
10 days earlier with progressive right hemipareses and unresponsiveness. Contrast-enhanced temporal bone CT
(A) reveals destruction of bone adjacent to the sigmoid sinus secondary to osteomyelitis (black arrow). Noncontrast
axial T2-weighted scan (B) reveals bilateral tympanomastoid fluid (curved white arrows) consistent with acute tym-
panomastoiditis. The left sigmoid sinus (open arrows) is compressed and displaced away from the petrous bone by
an epidural abscess (asterisk). Contrast-enhanced T1-weighted axial (C) and coronal (D) scans confirm the presence
of the epidural abscess (asterisk) as well as severe compression and inflammation of the sigmoid sinus (white arrow-
heads). The epidural location of the abscess is confirmed on the coronal image because of its extension above and
below the tentorium (dashed white arrows) and displacement of the sigmoid sinus away from the skull. Note the
extensive infarction of the left cerebral hemisphere caused by cortical venous and vein of Labbe´ thrombophlebitis.
Imaging of Head and Neck Emergencies 233
diagnosis. Identification of dural venous throm- mucosal layer lining the mastoid air cells leading to
bosis is more complicated on MR imaging–MRV bony demineralization induced by local pressure
because the signal intensity of thrombus evolves and osteolytic enzymes. Dedicated temporal
over time with changes of the hemoglobin moiety, bone CT is the optimal imaging choice for identi-
cellular integrity, and relative protein/water con- fying this particularly aggressive form of acute
tent over time. For example, subacute thrombus mastoiditis and will demonstrate either partial or
may be indistinguishable from normally opacified complete absence of the bony septa. The treat-
sinus on postcontrast T1-weighted imaging as ment of coalescent mastoiditis usually requires
well as hypointense flow voids on T2-weighted surgical drainage in addition to antibiotic therapy,
imaging (see Fig. 16). Therefore, in addition to so the distinction needs to be made from simple
conventional MR imaging, the authors adds 2D acute mastoiditis.25
and 3-dimensional phase contrast MRV to the im-
aging protocols. In some cases, acute otomastoiditis may extend
anteromedially to involve the petrous portion of the
Severe otomastoiditis can also progress along temporal bone. Petrous apicitis is essentially oste-
the septations of the mastoid process, resulting omyelitis of the petrous bone and may on occasion
in their eventual breakdown (coalescent mastoid- present as Gradenigo syndrome, with otorrhea,
itis) (see Figs. 15 and 16). This breakdown occurs facial pain or otalgia, and sixth cranial nerve palsy
when small microabscesses accumulate under the (Fig. 17). Associations with V1-branch trigeminal
Fig. 17. Gradenigo syndrome: Axial CT (A), sagittal noncontrast T1-weighted MR (B), and sagittal postcontrast T1-
weighted MR (C) images in a patient presenting with the triad of unilateral periorbital pain, sixth nerve palsy, and
otorrhea. Initial workup of otorrhea by CT revealed extensive petrous apicitis (white arrow) that progressed over
the next 2 weeks to the full triad of symptoms. Contrast-enhanced T1-weighted MR demonstrates diffuse
enhancement of the petrous apex (curved white arrow), cranial nerves within the internal auditory canal (dashed
white arrow), as well as faint enhancement of the preganglionic segment of the trigeminal nerve (white
arrowhead).
234 Brucker & Gentry
neuralgia and facial nerve palsy have also been re- Enhancement within the labyrinthine, canalicular,
ported, given the proximity of the petrous bone to and cisternal segments of the facial nerve should
the Meckel cave and the geniculate fossa, always be regarded as abnormal until proven
respectively.14,25 otherwise. In addition to infectious and inflamma-
tory causes of facial nerve or labyrinthine
Teaching point: Air-fluid levels anywhere in the enhancement, do not forget to consider schwan-
head and neck regions should raise suspicion of nomas, neuromas, ossifying hemangiomas, and
an acute infection, unless a different explanation perineural tumor spread.
can be found.
Idiopathic facial nerve palsy (Bell palsy)
Labyrinthitis and Facial Neuropathies (Fig. 18) is the most common cause of acute pe-
ripheral facial nerve dysfunction and is thought to
The clinical triad of otalgia, sensorineural hearing be viral in cause. It has a fairly distinct clinical pre-
loss, and vertigo in the acute setting should raise sentation and course, and imaging is not routinely
suspicion for inflammation of the inner ear and obtained if the clinical findings are straightfor-
the seventh and eighth cranial nerve complex. ward. MR imaging is useful in atypical cases for
Inflammatory are most readily visualized on MR excluding other causes of acute facial nerve palsy
imaging as abnormal enhancement along the (neoplasm, infarct, perineural tumor spread). Bell
course of the facial nerve and/or membranous palsy usually causes only minimal enlargement
labyrinthine structures. Enhancement within the of the nerve, enhances homogeneously, and ex-
geniculate and mastoid segments of the facial hibits no significant nodularity of the nerve. Any
nerve can be seen in normal patients. nodularity or significant focal enlargement of the
Fig. 18. Bell palsy: Axial (A, B) and coronal (C, D) contrast-enhanced T1-weighted images were obtained in this
patient who presented with a 2-day history of progressive right peripheral facial nerve palsy. The images reveal
marked enhancement of the geniculate (white arrows), tympanic, mastoid (white arrowheads), and parotid
(open black arrow) segments of the facial nerve. There should be no significant enlargement or nodularity of
the nerve in order to confidently make a diagnosis of Bell palsy.
Imaging of Head and Neck Emergencies 235
nerve would argue against Bell palsy as a cause Lyme disease, caused by the spirochete Borre-
(Fig. 19). lia burgdorferi, is another infectious cause of acute
facial nerve palsy, which can be confused with Bell
Another commonly encountered cause of acute palsy. The diagnosis often depends on a known
inflammatory facial nerve palsy is herpes zoster exposure history in an area that is endemic to
infection of the external ear and facial nerves. the Ixodes deer tick, which transmits the spiro-
This infection is termed herpes zoster oticus or chete to humans. The clinical presentation may
Ramsay-Hunt syndrome (Fig. 20). Imaging findings include arthralgias, erythema migrans rash, posi-
may mimic those of Bell palsy, although there is tive cerebrospinal fluid analysis, and involvement
often more cutaneous edema and other cranial of multiple cranial nerves.
nerves may be involved. Ramsay-Hunt syndrome
should also be clinically apparent in patients who Labyrinthitis refers to any inflammatory or infec-
presents with facial nerve palsy and painful vesi- tious condition that affects the membranous and
cles over the external ear and adjacent facial soft sensorineural portions of the inner ear. The most
tissues.25 Sometimes, however, the facial palsy common causes are viral and may be preceded
may predate the skin eruptions; the diagnosis by a stereotypical prodrome; but other forms of
may not be immediately obvious, and MR imaging the disease include autoimmune labyrinthitis,
may be required to make the diagnosis in an expe- vasculitis (eg, polyarteritis nodosa), and granulo-
ditious manner. matous disease (eg, granulomatosis with
Fig. 19. Bell palsy mimic (ossifying hemangioma): Axial T1-weighted (A), T2-weighted (B), and postcontrast T1-
weighted (C) MR images were obtained in this patient who presented with a 1-month history of progressive right
facial nerve palsy. The images reveal a T2 hypointense, contrast-enhancing mass in the region of the geniculate
ganglion (white arrows). The mass is obstructing the hypotympanum resulting in a mastoid effusion (curved
white arrows). This lesion is inconsistent with Bell palsy because of its masslike nature and prolonged 1-month
progression of the facial palsy.
236 Brucker & Gentry
Fig. 20. Ramsay-Hunt syndrome: Two patients with rapid onset of facial nerve palsy, otalgia, and vesicular skin erup-
tion over the ear indicating Ramsay-Hunt syndrome. Patient 1 (A): Contrast-enhanced T1-weighted image demon-
strates abnormal nonexpansile enhancement of the facial nerve genu (white open arrow) and greater superficial
petrosal nerve (white arrowhead). There is hazy enhancement of the cranial nerves within the internal auditory
canal (white arrow). The enhancement more consistent with a viral neuritis other than Bell palsy. Patient 2 (B–D):
Contrast-enhanced T1-weighted axial (B, C) and coronal (D) MR images reveal very subtle enhancement of the facial
nerve genu (white dashed arrows). There is marked edema and enhancement of the soft tissues around the left ear
(curved white arrows) because of the presence of extensive vesicular eruption of the skin. This amount of soft tissue
involvement is not associated with Bell palsy and more suggestive of Ramsay-Hunt syndrome.
polyangiitis). Bacterial labyrinthitis is considerably contrast-enhanced CT scan of the neck, typically
less common but might be encountered in severe with the intention of uncovering some acute insult
cases of prolonged, intractable otomastoiditis. to the salivary glands, tonsils, or lymph nodes. It is
On imaging, abnormally decreased T2 signal important to investigate the patients’ relevant clin-
intensity of the perilymphatic labyrinthine struc- ical history for prior malignancies of the head and
tures may be seen in addition to postcontrast neck, prior surgical interventions, autoimmune dis-
enhancement.25,26 orders, or immunosuppression. In the following
section, the authors limits the discussion to sialoa-
Teaching point: Enhancement of the postgeni- denitis and tonsillitis, ranging from the acute in-
culate (postganglionic) segments of the facial flammatory stage to abscess formation. It should
nerve can be a normal finding. However, asym- be noted that cervical lymphadenopathy may
metric enhancement, nodularity, thickening, or follow a similar disease course, with features of
extension to the cisternal/canalicular portions of early inflammation followed by apparent suppu-
the nerve are suggestive of disease. ration and cavitation. It is not formally discussed
here because lymphadenopathy is often a non-
EMERGENCIES OF THE GLANDULAR TISSUES specific finding, often accompanying other cervi-
cal infections caused by reactive changes or,
A clinical history of painful neck mass or throat in some cases, malignancy masquerading as
pain will usually prompt the acquisition of a
Imaging of Head and Neck Emergencies 237
infection. In short, abnormal lymph nodes need associated with facial paresis and taste distur-
to be followed to resolution or biopsied if still bances, secondary to inflammatory changes of
abnormal after completion of the treatment the facial nerve as it courses through the gland,
course. carrying with it efferent motor and afferent gusta-
tory nerve fibers. Further involvement of parasym-
Acute Sialoadenitis pathetic fibers within the chorda tympani and
lingual nerves may also contribute to submandib-
There is a wide range of pathologic conditions that ular and sublingual gland dysfunction.14,27–29
can lead to acute inflammatory changes of the
salivary glands, including various infections, radia- During the acute inflammatory phase, the imag-
tion therapy, facial trauma, autoimmune disorders, ing features of sialoadenitis are potentially non-
and ductal obstruction by calculi or neoplasms. specific, usually demonstrating a salivary gland
Despite the broad differential, patients with acute that is enlarged, edematous, and hyperenhancing
sialoadenitis usually present with similar symp- on both CT and MR imaging (Fig. 21). However,
toms: facial swelling and tenderness, salivary there are additional features that may help narrow
pain that is exacerbated by oral intake, and dry the differential, such as laterality, precontrast
mouth. Acute parotitis, specifically, can be attenuation pattern, evidence of ductal obstruc-
tion, and presence of sialoliths.
Fig. 21. Atypical mycobacterial sialadenitis and lymphadenitis: A 6-month-old child presenting to the emergency
department with fever, progressive neck swelling, and difficulty feeding. Axial (A, B) and coronal (C) contrast-
enhanced CT scans demonstrate extensive submandibular region suppurative lymphadenitis (white arrows)
with numerous small peripherally enhancing intranodal abscesses (white arrowheads). There is abnormal diffuse
homogeneous enhancement of the bilateral submandibular glands (curved black arrows) consistent with sialade-
nitis. The epidemiologic evidence suggests that infections like these are acquired from environmental sources,
including soil, water, dust, and aerosols. The differential diagnosis is broad and includes lymphadenitis caused
by mycobacterium tuberculosis, infectious mononucleosis, cat-scratch disease, brucellosis, actinomycosis, and
nocardiosis.
238 Brucker & Gentry
Most unilateral infectious sialoadenitis cases are attenuation surrounded by a thin rim of enhance-
secondary to bacterial infections, most often ment and inflamed surrounding glandular tissue
involving beta-hemolytic Streptococcus, Staphy- (see Fig. 21). Unfortunately, coalescent edema,
lococcus aureus, Streptococcus pneumonia, and nondrainable cellulitis, ductal and acinar dilatation,
atypical mycobacterial (see Fig. 21). Acute siala- and preexisting areas of hypoenhancing fibrosis
denitis is usually seen in the setting of an ob- can potentially mimic small abscess formation.
structing sialolith (80%–90% of cases). The Additional pitfalls include the presence of benign
submandibular gland is the most commonly in- cystic structures in the parotid glands, such as
volved salivary gland (70%–80% of cases), fol- lymphoepithelial cysts and first branchial cleft
lowed by the parotid gland (10%–20%); the cysts, although these may become secondarily in-
sublingual and minor salivary glands rarely fected to behave like abscesses, after all.
demonstrate primary involvement in acute in-
fectious sialoadenitis but may be secondarily Other patterns of salivary gland inflammation
inflamed. The submandibular glands are consid- suggest alternative causes of sialoadenitis. For
ered to be most susceptible to intraductal calculus example, bilateral salivary gland involvement is
formation and secondary sialoadenitis, owing to more suggestive of viral infection, radiation-
the relatively large size of the Wharton duct, small induced sialoadenitis, or an autoimmune disorder
papillary orifice, the ascending course of the duct (especially Sjo¨ gren syndrome). These conditions
into the floor of the mouth, higher viscosity of are not typically associated with enlargement
the secretions, and slower salivary flow rate. The of the extraglandular ducts, although there may
opposite can be said about the parotid be increased conspicuity of the intraglandular
gland.14,27–29 ducts secondary to inflammation and ductal
obstruction.14,27–29
In addition to the nonspecific imaging features
of acute inflammation, cases of acute bacterial Viral sialoadenitis is still most commonly caused
sialoadenitis can usually be confidently distin- by mumps (Paramyxovirus), especially in nonim-
guished from other causes of salivary gland dis- munized patients, although cases have been re-
ease and not just because it is the statistically ported with an assortment of viral causes,
most likely choice. Inflammatory changes of the including Influenza, Coxsackie, and Adenovirus.
submandibular or parotid gland that are unilateral, In these cases, one would expect to see marked
associated with dilation and enhancement of the pan-sialoadenitis in young patients with fever
salivary duct, and seen in the presence of a distal and other systemic symptoms of illness, without
obstructing calculus is diagnostic. CT is the specific evidence of bacterial or obstructive dis-
optimal modality for identifying calcified sialoliths, ease. The treatment of these patients is largely
which can be easily overlooked on MR imaging. supportive because the disease course is usually
Absence of calculi does not necessarily exclude limited.14,27–29
the diagnosis of obstructive sialoadenitis. Very
small calculi may be potentially obscured by Radiation sialoadenitis should be suspected in
dental artifacts or have already passed out of the any patient who has been administered radioac-
orifice by the time of the study. However, all cases tive iodine therapy (I-131) for thyroid disease or
of sialoadenitis in which an obstructing sialolith is any individual evaluated in the first several months
not identified will necessitate further follow-up for following external beam radiation therapy or head
any underlying malignant lesions of the oral and neck cancer. In the chronic phase, the glands
cavity.14,27–29 are often small and fibrotic, hyperdense on non-
contrast CT, and diffusely hyperenhancing on
The treatment of acute bacterial sialoadenitis postcontrast CT. The glands can be swollen,
usually entails a course of antibiotics with broad edematous, and hypodense on CT in the acute
enough coverage for any potential oral flora, setting, however. Hyperattenuation of the glands
robust hydration, and salivatory promoters (le- on noncontrast CT is a feature encountered espe-
mons). Small calculi, if present, will often pass on cially within the first days of I-131 administration
their own, although larger obstructing sialoliths because of the concentration of the radioiodine
may need to be surgically retrieved. Surgical within the salivary glands. The inflammatory
drainage may also be required in cases of abscess changes of the salivary glands are otherwise
formation. Sometimes gland excision is necessary nonspecific and treated with hydration, salivatory
if there is a history of recurrent/refractory acute/ stimulants, and antipyretics.14,27–29
chronic sialoadenitis.
Sjo¨ gren disease is a common autoimmune dis-
Making the diagnosis of salivary gland abscess order, characterized by B cell–mediated infiltration
can be problematic. The key imaging features and destruction of the lacrimal and salivary glands
are well-circumscribed focus of central low (particularly the parotid glands). These patients
may occasionally present with symptoms and
Imaging of Head and Neck Emergencies 239
signs of acute sialadenitis. It predominantly affects restricts diffusion on MR imaging, is concerning
female patients in the fourth to fifth decades of life. for lymphomatous involvement of the gland,
These patients classically present with dry mouth although rare cases of chronic sclerosing sialoa-
and dry eyes (keratoconjunctivitis sicca) and may denitis can also have this appearance.27,29
have a history of other autoimmune diseases,
such as lupus or rheumatoid arthritis, or various Teaching point: In the absence of a causative
forms of interstitial lung disease. Forty percent of sialolith, cases of sialoadenitis warrant further scru-
Sjo¨ gren disease cases are seen in isolation, how- tiny of potential underlying neoplastic disease.
ever.29 Aside from the patient demographics, early
Sjo¨ gren disease may be difficult to distinguish Tonsillitis
from viral sialoadenitis; but long-standing Sjo¨ gren
disease is usually notable on imaging for atrophic Acute tonsillitis is one of the most common infec-
salivary glands with heterogeneous, stippled tions of the head and neck, particularly among
attenuation, multiple small parotid cysts, and young patients. The most common causes are
numerous intraglandular sialoliths. In these pa- Epstein-Barr virus in adolescent patients as well
tients, it is important to be on the lookout for any as Staphylococcus aureus and Streptococcus
potential hypercellular masses because there is a species. The diagnosis is usually clinically
reported 44-times increased risk of developing apparent in these patients, who present with throat
lymphoma. An infiltrative lesion that is hyperen- pain, trismus, and tonsillar enlargement and ery-
hancing, isoattenuating to hyperattenuating to thema. Imaging is usually required in only the
muscle on CT, or relatively T2 hypointense and most severe cases in order to evaluate the extent
of disease and the presence of abscess.14
Fig. 22. Acute bilateral tonsillitis: Axial (A), coronal (B), and sagittal (C) contrast-enhanced CT scans demonstrate
severe bilateral enlargement of the palatine tonsils with linear streaks of hypodensity (black arrowheads) within
the tonsils representing pus-filled tonsillar crypts. Note the near-complete compromise of the pharyngeal airway
(white arrows) by the hypertrophied (kissing) tonsils.
240 Brucker & Gentry
On CT and MR imaging, acute tonsillitis mani- (see Fig. 22; Figs. 23 and 24). This fluid extension
fests as enlargement, edema, and hyperenhance- can, in turn, result in cellulitis or abscess formation
ment of the palatine tonsils, which may touch in within the parapharyngeal, masticator, and retro-
the midline oral cavity (kissing). On postcontrast pharyngeal spaces (see Fig. 24). Peritonsillar ab-
images, tonsillar inflammation may present with a scesses may also cause severe midline deviation
striated enhancement pattern, with parallel streaks of the tonsil and airway compromise (see Fig. 23).
of linear hypoenhancement representing areas of In contrast, a true tonsillar abscess results in an
edema, trapped fluid, and cellular debris accumu- area of liquefaction that is entirely contained by
lating within the tonsillar crypts (Fig. 22). Be careful the periphery of the gland and delineated by a
not to accidentally describe this finding as ab- thin rim of enhancement. It is important to indicate
scess formation, which would necessitate surgical the size of the abscess, as collections measuring
drainage. Similarly, focal areas of central hypoen- less than 1 cm may be too small to drain. Short-
hancement within the tonsillar tissues, without term clinical follow-up with adequate antibiotic
discrete peripheral rim enhancement, may repre- and supportive therapy, often as an inpatient,
sent devitalized nonliquefied suppurated tissue may be the preferred treatment option.30
that cannot be drained.14,30
CERVICAL SPACE EMERGENCIES
Tonsillitis-associated abscess comes in 2 flavors
(sorry, we couldn’t resist): (1) peritonsillar abscess, Not all painful, tender neck masses detected on
which is far more common, and (2) true tonsillar clinical examination turn out to be solid lesions.
abscess formation. With the former, an organized The layered arrangement of various fascial planes
area of inflammatory fluid extends beyond the coursing throughout the neck creates multiple
thin tonsillar capsule into the peritonsillar space
Fig. 23. Peritonsillar-retrotonsillar abscess: Axial (A), coronal (B), and sagittal (C) contrast-enhanced CT scans
demonstrate severe bilateral enlargement of the palatine tonsils caused by tonsillitis. There is a large rim-
enhancing abscess (star) displacing the ipsilateral tonsil (curved black arrows) medially and inferiorly.
Imaging of Head and Neck Emergencies 241
Fig. 24. Peritonsillar, retropharyngeal, and danger space abscesses: Axial (A, B), sagittal (C), and coronal (D)
contrast-enhanced CT scans demonstrate a multiloculated rim-enhancing peritonsillar abscess (stars) as well as
a large suppurative lateral retropharyngeal node (black arrows). The suppurative lymph node has ruptured
into the retropharyngeal space resulting in abscesses within the retropharyngeal (white arrows) and danger
space (black arrowheads) abscesses.
intervening spaces, which can potentially become spaces are difficult to treat medically and have
inoculated by bacteria and progress to severe the potential to affect to the adjacent visceral
cellulitis and myofasciitis (Figs. 25 and 26). Once structures or spread to other spaces within the
established, these infections of the deep cervical neck and mediastinum.
Fig. 25. Posterior cervical space necrotizing myofasciitis: Axial (A) and sagittal (B) contrast-enhanced CT scans
demonstrate extensive edema, skin thickening, gas formation (arrows), and abnormal enhancement of the pos-
terior cervical fascial planes and muscles in this patient with Streptococcus anginosus necrotizing myofasciitis.
242 Brucker & Gentry
Fig. 26. Necrotizing cervical–mediastinal fasciitis: Axial contrast-enhanced CT scans (A–D) reveal rapidly progres-
sive diffuse edema of the fascial planes and muscles in the neck and upper mediastinum (white arrows) in this
patient with early necrotizing fasciitis.
Floor of Mouth Infections direct extension from contagions of the masticator
buccal and parapharyngeal spaces as well as ex-
Most infections arising in the sublingual and sub- tracapsular extension of complicated submandib-
mandibular spaces are dental in origin. The 2 ular sialoadenitis.14,31
spaces are demarcated by the sling of the mylo-
hyoid muscle, which inserts on the mylohyoid With floor-of-mouth abscess formation, as with
line along the lingual margin of the mandible at any other infected fluid collection, one expects to
the approximate level of the mandibular dental find a nonenhancing low-attenuation fluid collec-
roots. Specifically, the roots of the first molar, pre- tion with peripheral rim enhancement, occasion-
molars, and canines terminate above the ridge; ally containing gas. With odontogenic causes of
dental infections of these teeth are prone to cause sublingual or submandibular abscess formation,
sublingual space infections (Figs. 27 and 28). The a subperiosteal abscess may also be seen. This
distal roots of the second and third mandibular abscess is seen as a sessile rim-enhancing low-
molar teeth extend below the mylohyoid line. attenuation collection with its base oriented longi-
Therefore, submandibular space infections should tudinally along the lingual margin of the mandible.
prompt for inspection of the second or third molar This part of the mandibular cortex must be in-
teeth for an odontogenic source. Submandibular spected for areas of osseous erosion and
space abscesses may also originate from sublin- dehiscence.
gual space infections that spread posterior to the
free margin of the mylohyoid muscle (see Fig. 27; Odontogenic submandibular space abscesses
Fig. 29) or directly through small defects in the will typically radiate out from the mandibular angle
muscular sling (boutonnie` re). Other causes include in an inferolateral direction, with subsequent
displacement of the submandibular gland and
Imaging of Head and Neck Emergencies 243
Fig. 27. Subperiosteal mandibular abscess, submandibular and sublingual space abscesses: Axial (A, B) and coro-
nal (C) contrast-enhanced CT scans demonstrate a rim-enhancing abscess abutting the lingual cortex of the
mandible (black arrows) adjacent to a periapical abscess of tooth 28 (not shown). Additionally seen are similar
rim-enhancing abscesses within the posterior portion of the sublingual space (curved black arrow) and subman-
dibular space (curved white arrow).
stranding of the submandibular fat. The outer and distension of the submandibular soft tissues
margin of the abscess may extend over the and upper throat.14,31
buccal and lingual cortical margins of the
mandible, potentially involving the mandibular fo- Retropharyngeal Abscess
ramen and by association the inferior alveolar
nerve. Extension of the abscess to involve the You will encounter various anatomic descriptions
buccal and masticator spaces is common (see of the retropharyngeal space, which can be a
Fig. 28). source of confusion when trying to distinguish a
retropharyngeal abscess from other infections
Ludwig angina is a specific type of severe head that have organized in the thin stretches of real es-
and neck infection that rapidly progresses tate sandwiched between the pharynx and cervi-
throughout the entire floor of the mouth, sublingual cal spine.
space, submandibular space, root of the tongue,
and pretracheal soft tissues (Fig. 30). These pa- The retropharyngeal space is defined anteriorly
tients present with glossal elevation and protru- by the buccopharyngeal fascia (a thin membrane
sion, difficulty controlling oral secretions, and that covers the dorsal margin of the pharyngeal
most importantly a threatened upper airway. constrictor muscles) and posteriorly by the alar
Although often seen in conjunction with abscess fascia. These two fascial layers and the intervening
and gas formation, it is technically only defined retropharyngeal space extend superiorly to the
by the presence of an aggressive cellulitis, which base of the skull where they attach separately.
on examination may manifest with painful firmness The buccopharyngeal and alar fascia fuse
244 Brucker & Gentry
Fig. 28. Masticator space abscess following recent dental extractions: Axial (A), coronal (B), and sagittal (C)
contrast-enhanced CT scans demonstrate recent extraction sockets (white arrows) of teeth 18 and 19. There is
a centrally hypointense rim-enhancing abscess (stars) involving the masseter and pterygoid musculature within
the masticator space.
inferiorly into a single layer thereby terminating upper airway. Severe or prolonged infections,
along the posterior margin of the esophagus at however, can promote bacterial seeding of the ret-
the T1-T2 level. At this level, the lower extent of ropharyngeal lymph nodes, which can then form
the retropharyngeal space is sometimes referred intranodal abscesses (suppuration). The rupture
to as the retrovisceral space and can communi- of suppurative retropharyngeal lymph nodes is
cate with the peritracheal space.14,30 A thin thought to be the pathogenesis of most retrophar-
sagittal fibrous band (the median raphe) extends yngeal abscesses (see Fig. 24). Initially the ab-
from the midline alar fascia and effectively divides scess will remain unilateral, bounded medially by
the retropharyngeal spaces into 2 lateral compo- the median raphe of the alar fascia. However, the
nents, each housing its respective half of the retro- alar fascia is very thin and infection can easily
pharyngeal lymphatic drainage system. breakthrough to the contralateral retropharyngeal
space or posteriorly into the danger space (see
The retropharyngeal lymph nodes are respon- Fig. 24).14,30
sible for draining the middle ears, eustachian
tubes, paranasal sinuses, and upper pharyngeal Retropharyngeal abscess must be differentiated
soft tissues in very young children. The retrophar- from acute calcific prevertebral tendinitis (Fig. 31),
yngeal lymphatic chains usually become mostly which is a painful inflammatory process that af-
obliterated within the first decade of life by fects the superior inserting fibers of the preverte-
repeated pharyngeal infections. In young patients, bral musculature, namely, the longus colli and
enlargement of retropharyngeal lymph nodes is longus capitis muscles. These muscles course
rather nonspecific and may be encountered in along the anterior margin of the cervical vertebral
the setting of any inflammatory process of the column and play a role in stabilizing movements
Imaging of Head and Neck Emergencies 245
Fig. 29. Masticator space abscess following recent dental extractions: Axial soft tissue (A), coronal soft tissue (B),
and bone (C) algorithm images demonstrate a periapical abscess of tooth 18 (curved white arrow) that has
eroded through the lingual cortex of the mandible. There is an abscess (black arrows) located within the subman-
dibular space inferior and lateral to the left mylohyoid muscle (white arrowheads). When there is cortical break-
through of an abscess below the attachment of the mylohyoid muscle to the mylohyoid line of the mandible
(black arrowheads), the abscess will occur in the submandibular space. The distal roots of the second and third
mandibular molar teeth typically extend below this line. Note the attachment of the contralateral mylohyoid
muscle (open white arrows) to the mylohyoid line.
of the head and neck. The longus colli muscles Descending Mediastinitis
insert superiorly along the anterior arch of the C1
vertebral body, and the longus capitis muscles The danger space is a potential space that ex-
insert along the base of the clivus. The inflamma- tends from the skull base superiorly down into
tory component of acute calcific prevertebral the retroesophageal mediastinum (see Fig. 26). It
tendinitis is incited by the presence of hydroxyap- is defined anteriorly by the alar fascia and posteri-
atite crystal deposition within the muscle fibers. orly by the prevertebral fascia, which invests the
On imaging, the classic features are a low attenu- longus colli and capitis muscles along the anterior
ation effusion within the prevertebral space, margin of the cervical spine. Infections within the
without peripheral rim enhancement or loculation, retropharyngeal space can permeate the alar fas-
and seen in the presence of calcification among cia and extend directly into the danger space.
the superior insertions of the prevertebral muscles. Danger space infections, with the aid of gravity,
The noncalcified portions of these muscles may can descend unimpeded into the mediastinum re-
appear hyperenhancing and edematous, and sulting in mediastinitis. This condition is potentially
regional reactive lymphadenopathy can also be life threatening and can be associated with severe
seen. sepsis and cardiovascular collapse. Treatment
246 Brucker & Gentry
Fig. 30. Ludwig angina: Oblique sagittal (A), axial (B, C), and coronal (D, E) contrast-enhanced CT scans demon-
strate multiple dental caries and periapical abscesses (curved black closed arrows) of the molar teeth. There is
extensive cellulitis and abnormal enhancement involving the sublingual and submandibular spaces. A crescent-
shaped abscess (straight black arrows) is present in the sublingual space just superior to the mylohyoid muscle
(curved black open arrows).
usually includes surgical drainage and intensive actuality, any combination of these infections
care.14,32,33 may be present at the same time.
Descending mediastinitis is usually defined by In addition to mediastinal spread, infections
the presence of a preceding infection of the head that descend along the carotid sheath have the
or neck, as opposed to primary mediastinitis that potential of inducing direct injury to the carotid
is secondary to esophageal injury or other direct arteries and internal jugular veins. Therefore,
violation of the mediastinum. Other potential routes the carotid space should be simultaneously
for descending cervical infection into the medias- evaluated for evidence of venous occlusion sec-
tinum (see Fig. 26) include the pretracheal space ondary to infectious thrombophlebitis (Lemierre
(contiguous with the anterior-superior medias- syndrome) (Fig. 32), arterial occlusion, vasculitis,
tinum), carotid space (contiguous with the middle and mycotic pseudoaneurysm formation. Large
mediastinum), and the prevertebral space (con- pseudoaneurysms may result in actual or semi-
tiguous with the posterior mediastinum).14,32,33 contained rupture (carotid blowout injury) and
can occur in the setting of carotid space infec-
The prevertebral space is a potential space that tions, radiation therapy, prior surgery (Fig. 33),
runs along the anterior margin of the vertebral col- vasculitis (Fig. 34), trauma, and from direct inva-
umn, bordered posteriorly by the anterior longitu- sion by malignant neoplasms.34,35 The aftermath
dinal ligament and anteriorly by the prevertebral of carotid injuries can be catastrophic, possibly
fascia. Infections within this space are usually sec- leading to embolic phenomena, ischemic infarc-
ondary to direct extension from spondylodiscitis. tions, exsanguination, and death. The course of
Inflammatory changes within the vertebral bodies, treatment is determined by the cause of the
intervertebral disks, and perivertebral muscula- injury, its extent and location along the vessel,
ture can, therefore, help distinguish a prevertebral and the presence of intracranial collateral
space infection from an infection in the dan- flow. Depending on the situation, endovascular
ger space or retropharyngeal space.14,32,33 In
Imaging of Head and Neck Emergencies 247
Fig. 31. Calcific prevertebral tendinitis: Axial (A, B) and sagittal (C) contrast-enhanced CT scans were acquired in
this afebrile patient who presented to the emergency department with neck pain. There is evidence of nonen-
hancing fluid in the retropharyngeal space (curved white arrow) raising the possibility of an abscess. Note is
made, however, of calcifications (white arrows) within the tendinous insertion of the longus coli muscle suggest-
ing that the fluid is likely caused by calcific prevertebral tendinitis rather than a true abscess.
stent-graft repair or surgical sacrifice may be especially if there is any suspicion of anaphylaxis
performed. or other difficulties in maintaining oxygen satura-
tion levels. Radiographs and CT examinations
Teaching point: Infections of the retropharyngeal offer the advantage of fast scan times, excellent
space, danger space, and prevertebral space need delineation of the airways, and sensitivity for radi-
to be evaluated in the sagittal plane. In particular, opaque foreign bodies. Foreign bodies of the
danger space infections necessitate evaluation of esophagus (Fig. 35), hypopharynx, or tracheo-
the mediastinum, and prevertebral infections bronchial tree may also indirectly result in acute
necessitate evaluation of the cervical spine. or subacute airway compromise if there is second-
ary aspiration.
AIRWAY EMERGENCIES
Epiglottis
Of course, any problem that compromises the
airway is a potentially life-threatening emergency. Marked enlargement and edematous changes of
Therefore, patients with an acute upper airway the epiglottis and aryepiglottic folds should raise
complaint need to have their breathing issues alarm for epiglottitis (see Fig. 1), which threatens
addressed before being transferred to the radi- patency of the laryngeal airway. Infection is
ology suite for imaging. Intubation should be usually by Haemophilus influenzae or Strepto-
considered before any examination that requires coccus species and can be accompanied by
patients to be supine (ie, CT and MR imaging),
248 Brucker & Gentry
Fig. 32. Internal jugular vein septic thrombophlebitis, Lemierre syndrome (Fusobacterium necrophorum): Axial
(A, B) and coronal (C) contrast-enhanced neck CT scans as well as a coronal MIP image of the chest (D) were
acquired in this patient who presented with fever, headache, and progressive left neck swelling 1 week following
an episode of pharyngitis and tonsillitis. The study demonstrates extensive inflammation (black arrowheads)
surrounding the internal jugular and facial veins (curved black arrows). There is a lack of normal enhancement
and presence of gas in these veins (straight black arrows) consistent with septic venous thrombophlebitis, which
was caused by the organism Fusobacterium Necrophorum in this case. Lemierre syndrome is caused by suppura-
tive thrombophlebitis of the internal jugular vein and its branches caused by oropharyngeal infections, such as
tonsillitis and dental infections. Spread of the infection into the facial venous system leads to septic thrombosis
of the jugular vein. This patient also exhibited one of the dreaded complications of this syndrome, numerous sep-
tic pulmonary infarcts (D).
signs of edema, supraglottic laryngeal swelling, Laryngotracheal Angioedema
and diffuse cellulitis of the surrounding soft
tissues in severe cases. The classic description Generalized inflammatory changes to the mucosa
on lateral radiographs of the neck is the thumb and submucosal soft tissues of the upper airway
sign, representing bulbous enlargement of the can lead to varying degrees of luminal airway nar-
suprahyoid epiglottis. These patients are typically rowing and respiratory compromise. The imaging
young and present with dyspnea and fever. The features in these cases are nonspecific but easily
treatment is broad-spectrum antibiotic therapy recognized: circumferential thickening of the hy-
and airway protection, usually achieved via popharyngeal, glottic, and/or tracheal soft tissues
intubation.14 with subsequent narrowing and deformity of the
airway lumen. It should be noted that even relative
Imaging of Head and Neck Emergencies 249
Fig. 33. Enlarging cervical hematoma after neck dissection: Axial (A, B) and coronal (C, D) contrast-enhanced neck
CT scans of the neck performed 6 hours following selective neck for oropharyngeal squamous cell carcinoma. The
images demonstrates a huge bilobed, mostly hyperdense cervical hematoma (H). There are areas that are not hy-
perdense, however, indicating ongoing bleeding and unclotted blood (black arrows). There is focal irregularity of
external carotid artery branches (white arrowheads) and an area of contrast extravasation into an unclotted
portion of the hematoma (black open arrow).
minor changes in absolute luminal size can result cellulitis. Treatment is, therefore, directed toward
in significant changes in airflow. Luminal resis- to the underlying disease process, in addition to
tance increases by a factor that is inversely related supportive care and airway protection. Intubation
to the fourth power of the radius (eg, halving the or tracheotomy is often indicated.14,30
luminal diameter increases resistance 16-fold).
Furthermore, fluid and exudative debris secondary Teaching point: Inflammatory conditions of the
to airway inflammation can further contribute to airway have the potential to progress rapidly.
luminal obstruction. Recognition of these conditions needs to be
immediately followed by communication to the
Significant causes of laryngotracheal angioe- clinician, with anticipation of the possible need
dema include anaphylaxis, radiation injury, and for medical management of the airway.
250 Brucker & Gentry
Fig. 34. Multiple external carotid pseudoaneurysms, vasculitis: Axial (A) and sagittal (B) CT scans of the neck, cor-
onal contrast-enhanced MR angiography (MRA) (C), and right external carotid angiogram (ECA) (D) were ac-
quired in this patient with acute lymphocytic leukemia and an enlarging right parotid mass. The CT scans
demonstrate a ring-enhancing right parotid mass (white arrows) with an eccentric area of enhancement (white
arrowheads) that was not separable from the external carotid artery. An apparent left internal carotid artery
dissection and pseudoaneurysm (black arrow) is also seen just below the skull base. The contrast-enhanced
MRA reveals external (curved white arrow) and internal (curved black arrow) carotid artery pseudoaneurysms.
The ECA angiogram, obtained at the time of embolization, confirms a right ECA pseudoaneurysm (curved black
open arrow), which was associated with large-vessel vasculitis at pathology.
Imaging of Head and Neck Emergencies 251
Fig. 35. Esophageal foreign body (chicken bone): Axial (A), sagittal (B), and coronal (C) CT scans of the neck were
obtained on this physician who inadvertently swallowed a chicken bone. There is a Y-shaped bone (white arrows)
in the lumen of the upper esophagus without obvious mucosal penetration.
SUMMARY stable enough to tolerate the duration of the scan.
This added step of preimaging clearance should
The anatomy of the head and neck contains very entail a review of the patients’ presenting symp-
few structures that could be considered expend- toms and past medical history, which will also
able and, consequently, is exceptionally intolerant help to refine the study protocol and provide a
to infection, inflammation, and injury. Acute patho- clinical context in which to interpret the images.
logic processes in this body region, therefore, tend
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Index
Note: Page numbers of article titles are in boldface type.
A and cervical lymph nodes, 127 radiologic.theclinics.com
CBT. See Carotid body tumors
ABC. See Aneurysmal bone cysts. CCF. See Carotid-cavernous fistula.
ACC. See Adenoid cystic carcinoma. Cellulitis
ACF. See Anterior cranial fossa.
Adenoid cystic carcinoma and infiltrative disease, 66, 67
Central cemento-ossifying fibromas
of the oral cavity, 112
of the parotid space, 139, 140 in the oral cavity, 109
Airway Cephaloceles
emergencies of, 247–251
and epiglottis, 247, 248 and petrous apex, 31
and laryngotracheal angioedema, 248–251 Cerebrospinal fluid, 4–6
Alveolar ridge Cervical fascia
squamous cell carcinoma of, 86, 87
Ameloblastomas and perivertebral space, 163, 164
in the oral cavity, 109, 110 Cervical lymph nodes
Aneurysmal bone cysts
and perivertebral space, 172–174 anatomy of, 115–119
Anterior cranial fossa, 1, 2, 4, 5, 7 and calcified lymphadenopathy, 123, 124
Arteriovenous malformations and carcinoma of unknown primary, 129
of the head and neck, 201 and Castleman disease, 127
in the oral cavity, 105 and cystic lymphadenopathy, 125
AVM. See Arteriovenous malformations. and diffuse lymphadenopathy, 126, 127
drainage of, 119
B and imaging findings, 121, 122
imaging techniques for, 119–121
Bacterial sinusitis and Kikuchi disease, 127, 128
and sinonasal cavity emergencies, 228, 229 and Kimura disease, 127, 128
and matted lymphadenopathy, 125, 126
Benign tumors and necrotic lymphadenopathy, 124, 125
in the oral cavity, 107–110 and reactive lymphadenopathy, 122, 123
and Rosai-Dorfman disease, 127, 128
Branchial apparatus anomalies and squamous cell carcinoma, 128, 129
in children, 182–187 and suppurative lymphadenopathy, 123
imaging characteristics of, 186 Cervical spaces
and descending mediastinitis, 245–247
Buccal mucosa emergencies of, 240–247
squamous cell carcinoma of, 84 and floor of mouth infections, 242, 243
and retropharyngeal abscess, 243–245
Buccomasseteric region Cervical thymic remnants
anatomy of, 101 in children, 184, 185, 188, 189
imaging characteristics of, 188
C Cholesteatomas
and external auditory canal, 18, 20, 21
Capillary malformations Cholesterol granuloma
of the head and neck, 198, 199 and middle ear, 22
in the oral cavity, 104 and petrous apex, 31
Chondrosarcoma
Carotid body tumors and perivertebral space, 172
of the head and neck, 204 and petrous apex, 31, 32
and skull base, 11–13
Carotid-cavernous fistula Chordoma
and extraocular muscle enlargement, 59–61 and perivertebral space, 172
Carotid sheath
imaging of, 140–142
Castleman disease
Radiol Clin N Am 53 (2015) 253–260
http://dx.doi.org/10.1016/S0033-8389(14)00176-6
0033-8389/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
254 Index and sinonasal lesions, 55
and subperiosteal hemorrhage, 54, 55
Chordoma (continued ) Extraocular muscle enlargement
and skull base, 10, 11 and carotid-cavernous fistula, 59–61
and dystrophic optic neuropathy, 58, 59
CM. See Capillary malformations. and idiopathic orbital inflammation, 59
CN. See Cranial nerves. and lymphoproliferative disease, 63
Combined vascular malformations and metastasis, 63
and sarcoidosis, 61–63
in the oral cavity, 105 and thyroid-associated orbitopathy, 58, 59
Common pediatric head and neck congenital/ and trauma, 63
developmental anomalies, 181–196 F
Congenital lesions
Facial neuropathies
in the oral cavity, 102–105 and temporal bone emergencies, 234–236
CP. See Cribriform plate.
Cranial nerves, 1–4, 9, 10 FD. See Fibrous dysplasia.
Cribriform plate, 1, 2, 4 FDG-PET. See Fluorodeoxyglucose-positron
CS. See Carotid sheath.
CSF. See Cerebrospinal fluid. emission tomography.
FE. See Fovea ethmoidalis.
D Fibro-osseous lesions
Dermoid cysts in the oral cavity, 108, 109
and extraconal lesions, 51 Fibromatosis
in the oral cavity, 105
in the oral cavity, 108
Descending mediastinitis Fibromatosis colli
and cervical space emergencies, 245–247
in children, 185, 186, 189, 190
Differentiated thyroid carcinomas, 152, 155, 157 imaging characteristics of, 190
Digital subtraction angiography Fibrous dysplasia
in the oral cavity, 109
and vascular lesions, 177 and skull base, 5, 6
Discitis Floor of the mouth
anatomy of, 100, 101
and perivertebral space, 167, 168 infections of, 242, 243
DON. See Dystrophic optic neuropathy. squamous cell carcinoma of, 84
DSA. See Digital subtraction angiography. Fluorodeoxyglucose-positron emission tomography
DTC. See Differentiated thyroid carcinomas. and thyroid cancer, 158
Dystrophic optic neuropathy FOM. See Floor of the mouth.
Foramina
and extraocular muscle enlargement, 58, 59 of the skull base, 1–4, 7, 9–12
Fovea ethmoidalis, 1, 6
E Fungal sinusitis
and sinonasal cavity emergencies, 229, 230
EAC. See External auditory canal.
Endolymphatic sac tumors G
and inner ear, 27 GCT. See Giant cell tumors.
Endophthalmitis Giant cell tumors
and intraocular masses, 76, 77 and perivertebral space, 174, 175
Epidermoid cysts Gingivobuccal region
in the oral cavity, 105 anatomy of, 101
Epiglottis GJT. See Glomus jugulare tumors.
Glandular tissues
and airway emergencies, 247, 248
Epistaxis and acute sialoadenitis, 237–239
emergencies of, 236–240
and sinonasal cavity emergencies, 230 and tonsillitis, 239, 240
External auditory canal Glomus jugulare tumors
imaging of, 204, 205
and cholesteatomas, 18, 20, 21
and necrotizing external otitis, 19
Extraconal lesions
and dermoid cysts, 51
and fibrous dysplasia, 54
and lacrimal gland lesions, 55–57
and lymphoproliferative lesions, 58
and orbital bone lesions, 51–55
and postseptal infection, 58
Index 255
and middle ear, 22–25 I
Glomus tympanicum
IAC. See Internal auditory canal.
and middle ear, 22–25 Idiopathic orbital inflammation
Glottis
and extraocular muscle enlargement, 59
squamous cell carcinoma of, 92, 93 and infiltrative disease, 65
Goiter and optic nerve sheath complex lesions, 42
Imaging evaluation of the suprahyoid neck, 133–144
imaging of, 148 Imaging of head and neck emergencies, 215–252
Graves disease Imaging of head and neck lymph nodes, 115–132
Imaging of the oral cavity, 99–114
and hyperthyroidism, 149, 151, 152 Imaging of the perivertebral space, 163–180
Imaging of the skull base: Anatomy and pathology,
H 1–14
Imaging of the temporal bone, 15–36
Hard palate Imaging of vascular lesions of the head and neck,
squamous cell carcinoma of, 87 197–213
Imaging thyroid disease: Updates, imaging
Head and neck approach, and management pearls, 145–161
and arteriovenous malformations, 201 Incidental thyroid nodules
and capillary malformations, 198, 199 imaging of, 146–148
and carotid body tumors, 204 Infantile hemangioma
emergencies of, 215–251 imaging characteristics of, 191
and glomus jugulare tumors, 204, 205 Infection
and hemangioma, 201–203 in the oral cavity, 105–107
imaging techniques for, 216–220 in the perivertebral space, 167
and juvenile nasopharyngeal angiofibroma, Infiltrative disease
206–210 and cellulitis, 66, 67
lymphadenopathy in, 122–128 and idiopathic orbital inflammation, 65
and lymphatic malformations, 199–201 and lymphoproliferative disease, 65
pediatric anomalies of, 181–196 and metastasis, 63, 64
vascular lesions of, 197–210 and plexiform neurofibroma, 67
and vascular malformations, 198–201 and rhabdomyosarcoma, 68
and vascular tumors, 201–210 and sarcoidosis, 67
and venous malformations, 199 Inflammation
in the oral cavity, 105–107
Hemangioma and perivertebral space, 167
in children, 187–192 Inner ear
of the head and neck, 201–203 and endolymphatic sac tumors, 27
in the oral cavity, 103 and intralabyrinthine schwannomas, 27
and labyrinthitis, 27
Hematoma and otosclerosis, 26, 27
and perivertebral space, 179 and semicircular canal dehiscence, 27, 28
Internal auditory canal, 18, 27, 32–34
Hemoptysis Intraconal lesions
and sinonasal cavity emergencies, 230 and intraconal metastasis, 49–51
and lymphatic malformations, 46–48
Herpetic neuralgia and lymphoproliferative disease, 49, 50
and intratemporal facial nerve, 32–34 and orbital cavernous malformations, 45, 46
and schwannoma, 49
HM. See Hemangioma. and venous varix, 49
HPV. See Human papilloma virus. Intralabyrinthine schwannomas
Human papilloma virus and inner ear, 27
Intraocular masses
and squamous cell carcinoma, 81, 85, 87, 88 and endophthalmitis, 76, 77
Hyperthyroidism and metastasis, 68
and retinal detachment, 69, 70
and Graves disease, 149, 151, 152
imaging of, 148–152
and role of radioactive iodine ablation, 151, 152
and role of radioactive iodine uptake scan,
150–153
Hypopharyngeal carcinoma
and anatomic considerations, 93
and demographic factors, 93, 94
and epidemiologic factors, 93, 94
and imaging manifestations, 94–96
256 Index matted, 125, 126
necrotic, 124, 125
Intraocular (continued ) rare diseases, 127, 128
and retinoblastoma, 71–76 reactive, 122, 123
and uveal melanoma, 70, 71 suppurative, 123
Lymphangiomas
Intratemporal facial nerve in the oral cavity, 105
and herpetic neuralgia, 32–34 Lymphatic malformations
and perineural tumor spread, 34 of the head and neck, 199–201
and venous malformations, 34 and intraconal lesions, 46–48
in the oral cavity, 105
IOI. See Idiopathic orbital inflammation. Lymphoproliferative disease
ITN. See Incidental thyroid nodules. and extraocular muscle enlargement, 63
and infiltrative disease, 65
J and intraconal lesions, 49, 50
and optic nerve sheath complex lesions, 42, 43
JNA. See Juvenile nasopharyngeal angiofibroma. Lymphoproliferative lesions
Juvenile nasopharyngeal angiofibroma and extraconal lesions, 58
imaging of, 206–210 M
K Malignant tumors
in the oral cavity, 110–112
Kikuchi disease
and cervical lymph nodes, 127, 128 Masticator space
imaging of, 135–138
Kimura disease
and cervical lymph nodes, 127, 128 Mastoid air cells, 20–26
MCF. See Middle cranial fossa.
L MEC. See Mucoepidermoid carcinoma.
Meningioma
Labyrinthitis
and inner ear, 27 and skull base, 7–9
and temporal bone emergencies, 234–236 Mesotympanum, 16
Metastasis
Lacrimal gland lesions
and extraconal lesions, 55–57 and extraocular muscle enlargement, 63
and infiltrative disease, 63, 64
Laryngeal carcinoma and intraconal lesions, 49–51
and anatomic considerations, 88–93 and intraocular masses, 68
and perivertebral space, 171–172
Laryngotracheal angioedema and skull base, 7
and airway emergencies, 248–251 Middle cranial fossa, 4, 5, 7
Middle ear
LCT. See Longus colli tendinitis. and cholesterol granuloma, 22
Lemierre syndrome and glomus jugulare tumors, 22–25
and glomus tympanicum, 22–25
and perivertebral space, 168, 169 and otitis media, 21, 22
Lingual thyroid and otomastoiditis, 21, 22
MS. See Masticator space.
in the oral cavity, 103 Mucoepidermoid carcinoma
Lingual tonsil of the oral cavity, 112
of the parotid space, 139
squamous cell carcinoma of, 88
Lips N
anatomy of, 101 Nasopharyngeal carcinoma
squamous cell carcinoma of, 84 and anatomic considerations, 82
LM. See Lymphatic malformations. and demographic factors, 82
Longus colli tendinitis and epidemiologic factors, 82
and perivertebral space, 169–171
Ludwig’s angina
in the oral cavity, 106, 107
Lymph nodes
of the head and neck, 115–129
Lymphadenopathy
calcified, 123, 124
cystic, 125
diffuse, 126, 127
in the head and neck, 122–128
Index 257
and imaging manifestations, 82, 83 and fibro-osseous lesions, 108, 109
of the pharyngeal mucosal space, 142, 144 and fibrous dysplasia, 109
and skull base, 6, 7 and hemangioma, 103
Necrotizing external otitis imaging of, 99–113
and external auditory canal, 19 and infection, 105–107
Necrotizing otitis externa and inflammation, 105–107
and temporal bone emergencies, 230, 231 and lingual thyroid, 103
NEO. See Necrotizing external otitis. and Ludwig’s angina, 106, 107
Nerve sheath tumors and lymphangiomas, 105
and perivertebral space, 176 and lymphatic malformations, 105
and skull base, 9, 10 malignant tumors in, 110–112
Neurofibroma and mucoepidermoid carcinoma, 112
and perivertebral space, 175, 176 and odontogenic keratocysts, 109
Neurofibromatosis type 1 and odontogenic lesions, 109
in children, 189–193 and pleomorphic adenomas, 107
imaging characteristics of, 192 and ranula, 107
NFI. See Neurofibromatosis type 1. and second branchial cleft cysts, 102
NPC. See Nasopharyngeal carcinoma. and soft tissue tumors, 107
NST. See Nerve sheath tumors. squamous cell carcinoma of, 83–87, 110, 111
and suprahyoid thyroglossal duct cysts, 102,
O
103
OC. See Oral cavity. vascular lesions in, 103
OCM. See Orbital cavernous malformation. and vascular malformations, 103, 104
Odontogenic keratocysts and vascular tumors, 103
and venous malformations, 104
in the oral cavity, 109 Orbit
Odontogenic lesions emergencies of, 220–228
imaging of, 37–78
in the oral cavity, 109 penetrating injuries of, 221–225
ONSC. See Optic nerve sheath complex. Orbital anatomy
ONSM. See Optic nerve sheath meningioma. axial, 38
OPG. See Optic pathway glioma. coronal, 39
Optic nerve sheath complex lesions sagittal, 39
Orbital bone lesions
and idiopathic orbital inflammation, 42 and extraconal lesions, 51–55
and lymphoproliferative disease, 42, 43 Orbital cavernous malformations
and optic nerve sheath meningioma, 43–45 and intraconal lesions, 45, 46
and optic neuritis, 40, 41 Orbital cellulitis
and optic pathway glioma, 45 and head and neck emergencies, 225, 227
and sarcoidosis, 45 Orbital imaging: A pattern-based approach, 37–80
Optic nerve sheath meningioma Orbital inflammation
and optic nerve sheath complex lesions, 43–45 noninfectious, 227, 228
Optic neuritis Oropharyngeal carcinoma
and optic nerve sheath complex lesions, 40, 41 and anatomic considerations, 87
Optic pathway glioma and demographic factors, 87, 88
and optic nerve sheath complex lesions, 45 and epidemiologic factors, 87, 88
Oral cavity Osteochondroma
and adenoid cystic carcinoma, 112 and perivertebral space, 172
and aggressive fibromatosis, 108 Osteomyelitis
and ameloblastomas, 109, 110 and perivertebral space, 167, 168
anatomy of, 99–101 Otitis media
and arteriovenous malformations, 105 and middle ear, 21, 22
benign tumors in, 107–110 Otomastoiditis
and capillary malformations, 104 and middle ear, 21, 22
and central cemento-ossifying fibromas, 109 and temporal bone emergencies, 231–234
and combined vascular malformations, 105 Otosclerosis
congenital lesions in, 102–105 and inner ear, 26, 27
and dermoid cysts, 105
and epidermoid cysts, 105
258 Index
P Pharyngeal mucosal space
imaging of, 142–144
Palatine tonsil and nasopharyngeal carcinoma, 142, 144
squamous cell carcinoma of, 87, 88 and squamous cell carcinoma, 144
Paragangliomas Pituitary adenoma
and skull base, 10 and skull base, 7
Parapharyngeal space Pleomorphic adenomas
imaging of, 134, 135 in the oral cavity, 107
Paraspinal space Plexiform neurofibroma
and perivertebral space, 165–167 and infiltrative disease, 67
Parotid space PMS. See Pharyngeal mucosal space.
and adenoid cystic carcinoma, 139, 140 PNF. See Plexiform neurofibroma.
imaging of, 138–140 PNTS. See Perineural tumor spread.
and mucoepidermoid carcinoma, 139 Postcricoid region
PCF. See Posterior cranial fossa. squamous cell carcinoma of, 95
Pediatric head and neck anomalies Posterior cranial fossa, 4, 5, 7
Posterior hypopharyngeal wall
and branchial apparatus anomalies, 182–187
and cervical thymic remnants, 184, 185, 188, 189 squamous cell carcinoma of, 95, 96
and fibromatosis colli, 185, 186, 189, 190 Posterior pharyngeal wall
and infantile hemangioma, 187–192
and neurofibromatosis type 1, 189–193 squamous cell carcinoma of, 88
and retinoblastoma, 193–195 Postseptal infection
and thyroglossal duct cysts, 182–184
Perineural tumor spread and extraconal lesions, 58
and intratemporal facial nerve, 34 PPS. See Parapharyngeal space.
Perivertebral space Prevertebral space
anatomy of, 163
and aneurysmal bone cysts, 172–174 and perivertebral space, 164, 165
and chondrosarcoma, 172 PS. See Parotid space.
and chordoma, 172 PVS. See Perivertebral space.
and discitis, 167, 168 Pyriform sinus
and disease localization, 167
and fascial layers, 163, 164 squamous cell carcinoma of, 94, 95
and giant cell tumors, 174, 175
and hematoma, 179 R
imaging of, 163–179
and infection, 167 Radioactive iodine ablation
and inflammation, 167 and hyperthyroidism, 151, 152
and Lemierre syndrome, 168, 169 and thyroid cancer, 155–158
and longus colli tendinitis, 169–171
and malignant peripheral nerve sheath tumor, 176 Radioactive iodine uptake scan
and metastatic disease, 171–172 and hyperthyroidism, 150–153
and neurofibroma, 175, 176
and osteochondroma, 172 RAI. See Radioactive iodine.
and osteomyelitis, 167, 168 RAIU. See Radioactive iodine uptake.
and paraspinal space, 165–167 Ranula
and prevertebral space, 164, 165
and schwannoma, 175 in the oral cavity, 107
and spondylodiscitis, 167, 168 RB. See Retinoblastoma.
and tumors of nervous tissue origin, 175, 176 RD. See Retinal detachment.
and tumors of osseous origin, 171–175 Retinal detachment
and vascular lesions, 176–179
and vertebral artery dissection, 177, 178 and intraocular masses, 69, 70
Petrous apex Retinoblastoma
and cephaloceles, 31
and cholesterol granuloma, 31 in children, 193–195
and chondrosarcoma, 31, 32 imaging characteristics of, 194
and intraocular masses, 71–76
Retropharyngeal abscess
and cervical space emergencies, 243–245
Rhabdomyosarcoma
and infiltrative disease, 68
RMS. See Rhabdomyosarcoma.
Rosai-Dorfman disease
and cervical lymph nodes, 127, 128
Index 259
S tumorlike disorders of, 5, 6
SOF. See Superior orbital fissure.
Sarcoidosis Soft palate
and extraocular muscle enlargement, 61–63
and infiltrative disease, 67 squamous cell carcinoma of, 88
and optic nerve sheath complex lesions, 45 Soft tissue tumors
SCCa. See Squamous cell carcinoma. in the oral cavity, 107
Schwannoma SPH. See Subperiosteal hemorrhage.
Spondylodiscitis
and intraconal lesions, 49
and perivertebral space, 175 and perivertebral space, 167, 168
Second branchial cleft cysts Squamous cell carcinoma
in the oral cavity, 102
Semicircular canal dehiscence of the alveolar ridge, 86, 87
and inner ear, 27, 28 of the buccal mucosa, 84
Sialoadenitis and cervical lymph nodes, 128, 129
and glandular tissue emergencies, 237–239 of the floor of the mouth, 84
Sinonasal cavity of the glottis, 92, 93
and acute bacterial sinusitis, 228, 229 of the hard palate, 87
and acute invasive fungal sinusitis, 229, 230 and human papilloma virus, 81, 85, 87, 88
emergencies of, 228–230 hypopharyngeal, 93–96
and epistaxis, 230 laryngeal, 88–93
and hemoptysis, 230 of the lingual tonsil, 88
Sinonasal lesions of the lip, 84
and extraconal lesions, 55 nasopharyngeal, 82, 83
Sinonasal tumors of the oral cavity, 83–87, 110, 111
and skull base, 6 oropharyngeal, 87, 88
Skull base of the palatine tonsil, 87, 88
anatomy of, 1–4 of the pharyngeal mucosal space, 144
anterior anatomy, 1, 2 of the postcricoid region, 95
and anterior cranial fossa, 1, 2, 4, 5, 7 of the posterior hypopharyngeal wall, 95, 96
and cerebrospinal fluid, 4–6 of the posterior pharyngeal wall, 88
and chondrosarcoma, 11–13 of the pyriform sinus, 94, 95
and chordoma, 10, 11 of the soft palate, 88
communication pathways of, 2 staging of, 81, 82
congenital disorders of, 4 of the subglottis, 93
and cranial nerves, 1–4, 9, 10 of the supraglottis, 90–92
and cribriform plate, 1, 2, 4 of the tongue, 84–86
crossing structures of, 2 Squamous cell carcinoma of the upper aerodigestive
disorders of, 4–13 tract: A review, 81–97
and fibrous dysplasia, 5, 6 Subglottis
foramina of, 1–4, 7, 9–12 squamous cell carcinoma of, 93
and fovea ethmoidalis, 1, 6 Sublingual space
infectious disorders of, 4, 5 anatomy of, 101
and invasive pituitary adenoma, 7 Submandibular space
and meningioma, 7–9 anatomy of, 101
and metastases, 7 Subperiosteal hemorrhage
middle anatomy, 2–4 and extraconal lesions, 54, 55
and middle cranial fossa, 4, 5, 7 Superior orbital fissure, 3
and nasopharyngeal carcinoma, 6, 7 Supraglottis
neoplastic disorders of, 6–13 squamous cell carcinoma of, 90–92
and nerve sheath tumors, 9, 10 Suprahyoid neck
and paragangliomas, 10 imaging of, 133–144
posterior anatomy, 4 Suprahyoid thyroglossal duct cysts
and posterior cranial fossa, 4, 5, 7 in the oral cavity, 102, 103
and sinonasal tumors, 6
and superior orbital fissure, 3 T
traumatic disorders of, 4 TAO. See Thyroid-associated orbitopathy.
260 Index
Temporal bone anatomy of, 99, 100
and acute otomastoiditis, 231–234 squamous cell carcinoma of, 84–86
anatomy of, 16–18 Tonsillitis
emergencies of, 230–236 and glandular tissue emergencies, 239, 240
and external auditory canal, 16, 18–22 Trauma
and facial neuropathies, 234–236 and extraocular muscle enlargement, 63
and imaging techniques, 15, 16 Tympanic membrane, 16, 18, 20
and inner ear, 26–28
and internal auditory canal, 18, 27, 32–34 U
and intratemporal facial nerve, 32–34
and labyrinthitis, 234–236 UM. See Uveal melanoma.
and mastoid air cells, 20–26 Uveal melanoma
and mesotympanum, 16
and middle ear, 16, 20–26 and intraocular masses, 70, 71
and necrotizing otitis externa, 230, 231
and petrous apex, 28–32 V
and tympanic membrane, 16, 18, 20
Vascular lesions
TGDC. See Thyroglossal duct cysts. and digital subtraction angiography, 177
Thyroglossal duct cysts imaging techniques for, 198
in the oral cavity, 103
in children, 182–184 and perivertebral space, 176–179
imaging characteristics of, 183
Thyroid-associated orbitopathy Vascular malformations
and extraocular muscle enlargement, 58, 59 of the head and neck, 198–201
Thyroid cancer in the oral cavity, 103, 104
and differentiated thyroid carcinomas, 152, 155,
Vascular tumors
157 of the head and neck, 201–210
imaging of, 146, 147, 152–159 in the oral cavity, 103
preoperative work-up of, 152–156
recurrent, 156–158 Venous malformations
and role of computed tomography, 153, 154 of the head and neck, 199
and role of fluorodeoxyglucose-positron emission and intratemporal facial nerve, 34
in the oral cavity, 104
tomography, 158
and role of MR imaging, 153, 154 Venous varix
and role of radioactive iodine ablation, 155–158 and intraconal lesions, 49
and role of ultrasonography, 153, 157
and role of whole-body scintigraphy, 157 Vertebral artery dissection
Thyroid disease and perivertebral space, 177, 178
imaging of, 145–159
Thyroid nodules VM. See Venous malformations.
imaging of, 146–148
risk categories for, 147 W
TM. See Tympanic membrane.
Tongue WBS. See Whole-body scintigraphy.
Whole-body scintigraphy
and thyroid cancer, 157
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