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Imaging Evaluation of Pediatric
Parotid Gland Abnormalities
Emilio J. Inarejos Clemente, MD
María Navallas, MD
Mirkamal Tolend, BsC
Mariona Suñol Capella, MD
Josep Rubio-Palau, PhD
Asteria Albert Cazalla, MD
Monica Rebollo Polo, MD
RadioGraphics 2018; 38:0000–0000
https://doi.org/10.1148/rg.2018170011
Content Codes:
From the Departments of Diagnostic Imaging
(E.J.I.C., M.N., M.R.P.), Pathology (M.S.C.),
and Maxillary and Oral Surgery (J.R.P., A.A.C.),
Hospital Sant Joan de Deu, Av. Sant Joan de
Deu 2, CP 08950 Esplugues de Llobregat
(Barcelona), Spain; and Department of Di-
agnostic Imaging, Hospital for Sick Children,
Toronto, Ontario, Canada (M.T.). Presented as
an education exhibit at the 2016 RSNA Annual
Meeting. Received February 16, 2017; revision
requested May 4 and received September 20;
accepted November 2. For this journal-based
SA-CME activity, the authors, editor, and re-
viewers have disclosed no relevant relationships.
Address correspondence to E.J.I.C. (e-mail:
emilioinarejos­@gmail.com).
© ©
RSNA, 2018
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
■■Recognize the normal anatomy of the
parotid space in children by using differ-
ent imaging techniques.
■■Describe the imaging protocol for
studying parotid gland lesions in chil-
dren.
■■Identify the radiologic patterns of man-
ifestation of the most frequent benign
and malignant lesions that may arise in
the parotid gland.
See rsna.org/learning-center-rg.
1
PEDIATRIC IMAGING
Parotid gland lesions in children can be divided into benign or ma-
lignant. The age of the patient helps narrow the differential diagno-
sis, with vascular and congenital lesions being more frequent in the
1st year of life, while solid tumors are more frequent in older chil-
dren. Inflammatory disease usually has rapid onset in comparison
with that of neoplastic or congenital processes, which have more
gradual clinical evolution. Currently, multiple imaging techniques
are available to study the parotid region, such as US, CT, and MRI.
However, it is still a challenge to distinguish nonmalignant lesions
from malignant ones. US is the first-line diagnostic approach in
children to characterize the morphology and vascularity of these le-
sions. CT in children may be indicated for evaluation of abscesses
or sialolithiasis. MRI is the imaging modality of choice for investi-
gating the nature of the lesion and its extent. In addition to com-
plete and detailed clinical information, knowledge of parotid gland
anatomy and characteristic radiologic features of parotid disorders
is essential for optimal radiologic evaluation and avoiding unneces-
sary interventional diagnostic procedures or treatment. This article
illustrates a variety of entities (congenital, inflammatory, vascular,
neoplastic) that can occur in the parotid gland, highlighting the
most frequent radiologic patterns of manifestation and correlating
them with clinical, surgical, and pathologic findings.
RSNA, 2018 • radiographics.rsna.org
Introduction
The parotid gland is the largest salivary gland in the body and is located
in the parotid space (1,2). A wide variety of salivary gland lesions have
been described in the pediatric literature, such as congenital anomalies,
inflammatory or infectious processes, and benign or malignant neo-
plasms (3,4). Nevertheless, salivary gland lesions are relatively uncom-
mon in children, and the vast majority of these are benign (Table 1).
The age of the patient narrows the potential differential diagnoses,
with vascular and congenital lesions occurring more frequently in the
1st year of life, while solid tumors tend to manifest in older children.
Inflammatory disease usually has relatively acute onset in compari-
son with that of neoplastic or congenital processes, which have more
insidious evolution. US, CT, and MRI may help characterize the
specific cause (5).
2 September-October 2018
TEACHING POINTS
■■ If a tubular cystic lesion within the parotid gland extends with
a sinus tract to the skin at the level of the angle of the man-
dible, a branchial cleft cyst should be considered.
■■ At US, the parotid gland may show diffuse and heteroge-
neous enlargement with foci of salivary secretions and lymph
nodes. These foci consist of a mixture of inflammatory exu-
date and saliva remaining partly obstructed within the alveoli
of the gland. At Doppler US, there is increased vascularization
of the gland. US is considered the standard of reference for
diagnosing acute parotitis.
■■ Sometimes, chronic parotitis may be unilateral, and the gland
may appear atrophic and diffusely hypoechoic with irregular
margins and small foci of calcification.
■■ When a lobulated well-defined mass has central necrosis,
pleomorphic adenoma should be considered in the differen-
tial diagnosis.
■■ At MRI, low-grade mucoepidermoid carcinoma can mimic
solid benign tumors, such as pleomorphic adenoma, and
therefore is often considered in the differential diagnosis.
Comprehension of clinical information,
normal anatomy, and imaging characteristics of
parotid gland disease is essential for appropri-
ate radiologic evaluation and to plan suitable
treatment.
In this article, we describe the embryology and
normal anatomy of the parotid space, its bound-
aries, and its relations and highlight the radio-
logic appearances of the most frequent benign
and malignant parotid lesions, correlating those
appearances with findings at gross specimen and
pathologic analysis.
Embryology
Between the 6th and 8th weeks of fetal develop-
ment, the parotid gland arises from the ectoderm
within the mouth, branching dorsally and crani-
ally toward the ear. At the same time, the facial
nerve and associated second arch musculature
migrate ventrally and caudally (6). The parotid
gland contains secretory parenchymal tissue, which
is of ectodermal origin for the parotid glands and
endodermal origin for the submandibular glands,
sublingual glands, and minor salivary glands. The
stroma of the glands develops from a mesodermal
origin, although an additional component migrating
from the neural crest has been postulated (1,6).
The glandular components emerge from a lo-
cal proliferation of oral epithelium, which cana-
lizes and forms ducts by the 10th week of gesta-
tion but does not start secreting enzymes until
the 18th week of gestation (6,7). The secretory
or parenchymal tissues of the gland all arise from
these proliferations of oral epithelium.
The parotid gland is unique in that it becomes
encapsulated after development of the lymphatic
radiographics.rsna.org
system, resulting in the presence of both intrapa-
rotid lymph nodes and lymphatic channels. This
contrasts with the submandibular gland, which
undergoes early encapsulation in embryogenesis
and is devoid of intraglandular lymph nodes (6,7).
Anatomy
The parotid space is surrounded anteriorly by the
masticator space and medially by the carotid and
parapharyngeal spaces (Fig 1). The superficial
layer of the deep cervical fascia splits to encom-
pass the parotid space (1). It contains the parotid
gland, retromandibular vein, facial nerve, external
carotid artery, and intraparotid lymph nodes (Fig
2) (1,2). Another classification of the parapha-
ryngeal space divides it into pre- and poststyloid
spaces, with the parotid gland lying in the presty-
loid parapharyngeal space.
The intraparotid facial nerve creates a surgi-
cal plane that divides the parotid gland into two
lobes: superficial and deep. The intraparotid fa-
cial nerve is difficult to identify at cross-sectional
imaging. The hypointense linear tracts seen on
axial T1-weighted MR images are most likely the
intraparotid ductal rami and not the facial nerve.
At imaging, the lobes may be divided by the
retromandibular vein into superficial and deep
lobes (5).
The parotid duct or Stensen duct drains the
entire gland. It emerges from the anterior pa-
rotid space, courses anteriorly over the surface
of the masseter muscle, then arches medially
through the buccal space to traverse the buccina-
tor muscle at the level of the upper (maxillary)
second molar (1). The parotid duct is frequently
not visualized if it is not dilated.
The normal parotid gland shows numerous
intraparenchymal lymph nodes. The lymph nodes
are found superficial to the parotid gland and
within the gland parenchyma (2).
To aid in planning appropriate surgical resec-
tion and avoid facial nerve injuries, the radiolo-
gist should specifically report whether a parotid
lesion is confined to the superficial or deep lobe
of the gland. The gland is accessed through a pre-
auricular-retrotragal approach, creating subcuta-
neous and superficial musculoaponeurotic system
(SMAS) flaps. Monitoring of the facial nerve,
especially of the branches, is crucial to reduce
injury during surgery. Identification and dissec-
tion of the facial nerve before surgery reduces the
probability of damaging it. The extent to which
the facial nerve must be dissected during superfi-
cial parotidectomy is variable.
Imaging Techniques
In children, the initial approach to evaluating
the parotid gland is US using high-resolution
RG • Volume 38 Number 5
Table 1: Differential Diagnosis of Parotid
Gland Lesions in Children
Congenital/developmental anomalies
First branchial arch anomalies
Inflammatory or infectious processes
Acute bacterial sialadenitis
Viral: parotitis (acute and chronic)
Chronic sclerosing sialadenitis
Mycobacterial disease
Vascular malformations
Combined venolymphatic malformation
Lymphatic malformation
Benign epithelial tumors
Pleomorphic adenoma
Dermoid cyst
Benign mesenchymal tumors
Infantile hemangioma
Neurogenic tumors: neurofibroma
Malignant tumors
Mucoepidermoid carcinoma
Lymphoma
Rhabdomyosarcoma
Metastases
linear-array transducers. The absence of ionizing
radiation, availability, speed, and lack of need
for sedation make US the initial examination of
choice for studying the parotid gland (8). The
role of B-mode and color Doppler US should
be considered as well in follow-up of the cases.
At US, the normal parotid gland demonstrates
numerous intraparenchymal lymph nodes, seen
as small well-defined areas of hypoechogenicity;
these should not be misinterpreted as pathologic
(Fig 3) (8,9).
CT is not considered the standard of refer-
ence technique for evaluating the parotid gland
in children, since the gland is of similar attenua-
tion as the adjacent soft tissue, making it difficult
to detect some lesions. Use of CT in children
is mostly indicated for acute processes such as
parotid gland abscesses or sialolithiasis (5), which
may manifest as fever, pain, and swelling of the
affected parotid gland, with worsening of symp-
toms when salivary flow is stimulated.
MRI is the standard of reference for charac-
terizing parotid lesions (10–12). A specific MRI
protocol targeted to the parotid region helps
better characterize parotid disorders (Table 2).
A routine standard protocol should include
anatomic sequences such as T1-weighted and
T2-weighted imaging, with and without fat sup-
pression, to identify and locate the lesion. Diffu-
sion-weighted imaging (DWI) and postcontrast
Inarejos Clemente et al 3
Figure 1. Normal radiologic anatomy of the parotid
space. Axial T2-weighted MR image shows the parotid
space (1), masticator space (2), carotid space (3), pa-
rotid gland (*), and retromandibular vein (arrow).
imaging help characterize the nature of the lesion
and its extent.
In comparison with the surrounding soft tis-
sue, the parotid gland shows similar echogenicity
at US, similar attenuation at CT, and similar
signal intensity at MRI.
Congenital Anomalies
First Branchial Cleft Cysts
Definition.—Branchial cleft cysts result from
persistence of branchial cleft remnants. They are
classified according to which cleft persists, with
the second cleft being the most common, fol-
lowed by the first and third (Fig 4) (1,3,13).
Clinical Features.—Branchial cleft cysts typically
manifest as recurrent tender masses, enlarg-
ing within days after an infection of the upper
respiratory tract or external ear (13,14). The cyst
may disappear at both physical examination and
imaging when treated early with antibiotics.
Epidemiology.—First branchial cleft anomalies
are rare, accounting for up to 8% of all branchial
anomalies; it has been reported in the literature
that 68% are cysts, 16% are sinuses, and 16% are
fistulas (1). They are classified as type I or type II,
depending on whether they are confined only to
the membranous external auditory canal (type I)
or occur primarily near the angle of the mandi-
ble, with the tract extending through the parotid
gland toward both the membranous and carti-
laginous external auditory canal (type II) (13,14).
4 September-October 2018 radiographics.rsna.org

Figure 2. Axial anatomic section through the parotid gland shows the normal parotid region.
CN = cranial nerve.

Figure 3. Normal parotid gland at

US. Transverse US image shows a nor-
mal parotid gland (1) and mandibu-
lar ramus (2). The gland is relatively
hyperechoic compared with the sur-
rounding soft tissue and demonstrates
several normal intraparenchymal
lymph nodes (3).

First branchial cleft cysts usually occur in the

preauricular region of the parotid gland and can
vary from 1 to 7 cm in diameter. They tend to
occur in the parotid space with painless swelling
and can also manifest with otorrhea owing to an
external auditory canal sinus tract (1,15).
Imaging Findings.—These are well-defined,
rounded, and cystic masses, most commonly
located within the parotid gland. At US, first
branchial cleft cysts usually manifest as cysts,
with a smooth thinned wall, but if there is com-
plication, such as hemorrhage or infection, the
capsule may be thickened and internal debris
can be identified (8–10). At Doppler examina-
tion, there will be peripheral hyperemia with no
evidence of internal flow. At CT, the cyst will
appear as a well-defined, rounded or tubular,
low-attenuation lesion with peripheral enhance-
ment after contrast material administration. At
MRI, the cyst is hypointense on T1-weighted
images and hyperintense on T2-weighted images
(Fig 5) (11,12,16).
However, when complication is present,
the cyst may show hemorrhage, septa, and
surrounding edema. Occasionally, there is a
fistula connecting the lesion with the skin at the
level of the angle of the mandible (Fig 5). If a
tubular cystic lesion within the parotid gland
extends with a sinus tract to the skin at the level
of the angle of the mandible, a branchial cleft
cyst should be considered. MR imaging is the
imaging modality of choice to better demon-
strate the extension of the fistula and to plan a
suitable surgery.
Histologic Findings.—The cysts and fistulous
tracts are usually lined by squamous epithelium,
but columnar and ciliated epithelium may also be
present (Fig 5) (12). Some of the cysts located in
the lower neck may contain mucinous, seromu-
cinous, and sebaceous glands. The tissue around
the cyst may contain lymphoid aggregates with
germinal centers and chronic inflammation.
Treatment.—Complete surgical resection of the
cyst or fistula, including the sinus track from the
skin to its origin, is mandatory (Fig 5). If the or-
igin is located in the auricular or tragal cartilage,
a small piece of the origin should be resected
to avoid relapse or recurrent infections (13,14).
RG • Volume 38 Number 5 Inarejos Clemente et al 5

Table 2: MRI Protocol for Study of the Parotid Region

TR FOV Section Thick- Acquisition

Sequence (msec) TE (msec) (cm) ness (mm) Matrix NSA Time (min:sec)
Axial T2W FSE 3000 85 16 3 224 × 224 2 3:20
Axial T2W FS FSE 3500 85 16 3 224 × 224 2 3:30
Coronal STIR 4300 50 18 4 224 × 224 1 4:25
Sagittal T2W FS 5500 85 18 4 224 × 224 2 3:30
Axial T1W FSE 630 Minimum 16 3 256 × 256 3 3:21
Axial DWI 8300 Minimum 16 3 128 × 128 3 3:03
Axial T1W FS Gd 540 Minimum 16 3 256 × 256 3 5:03
Coronal T1W FS Gd 600 Minimum 18 4 256 × 256 2 3:47
Note.—DWI = diffusion-weighted imaging, FOV = field of view, FS = fat-suppressed, FSE = fast spin-echo, Gd =
gadolinium-enhanced, NSA = number of signals acquired, STIR = short inversion time inversion-recovery, TE =
echo time, T1W = T1-weighted, TR = repetition time, T2W = T2-weighted.

Figure 4. Lateral oblique photograph

of a child shows the location of branchial
cleft cysts and fistulas from arches I to IV.
First branchial cleft cysts will always mani-
fest above the angle of the mandible and
in the preauricular region. * = sternoclei-
domastoid muscle.

the angle of the mandible and may be associated

with fever and leukocytosis (17,18).

Epidemiology.—Acute parotitis is the most com-

Saline and posterior injection of methylene blue
into the fistula are useful to clean the tract and
to ease the surgery.
Inflammatory Conditions
Acute Parotitis
Definition.—Acute inflammation of the parotid
gland is most commonly caused by infections.
In contrast, chronic parotitis may originate from
several different processes: autoimmune, infec-
tious, systemic, and neoplastic (17).
Clinical Features.—Acute parotitis tends to mani-
fest with painful facial swelling and tenderness at
mon pediatric parotid inflammatory disease.
Mumps usually causes bilateral parotitis, although
some cases may show unilateral involvement. Ra-
diographic evaluation is typically not required.
Bacterial sialadenitis is exceptionally common
in children, and the parotid is the most frequent
salivary gland to be affected, with Staphylococcus
aureus being the most common pathogen. Suppu-
rative parotitis frequently affects premature infants
(35%–40% of cases) and immunosuppressed
children, with dehydration being the main predis-
posing factor (19–21).
Imaging Findings.—At imaging, inflamed sali-
vary glands are often enlarged, with their borders
ranging from well-defined to poorly defined. The
majority of cases tend to be heterogeneous at all
imaging modalities.
At US, the parotid gland may show diffuse and
heterogeneous enlargement with foci of salivary
secretions and lymph nodes (Fig 6). These foci con-
sist of a mixture of inflammatory exudate and saliva
remaining partly obstructed within the alveoli of the
gland. At Doppler US, there is increased vascular-
ization of the gland (Fig 6). US is considered the
standard of reference for diagnosing acute parotitis.
The role of CT may be limited to character-
ization and extension of intraparotid abscesses,
6 September-October 2018 radiographics.rsna.org

Figure 5. First branchial cleft cyst involving the superficial lobe of the left parotid gland in a 5-year-old boy.
(a) Sagittal oblique T2-weighted MR image shows a hyperintense tubular structure with a thickened wall in the
parotid gland, extending from the level of the auditory canal (*) to the skin (arrow), consistent with a fistula.
(b) Coronal T2-weighted MR image confirms external fistulization of the lesion (arrow). (c) Photograph shows
surgical dissection of the fistula (arrow). Results of physical examination confirmed the fistula to be at the level of
the angle of the mandible, narrowing the differential diagnosis at MRI. (d) Low-power photomicrograph shows a
combination of squamous and columnar ciliated epithelium (black arrow) in a background of inflammatory com-
ponent (*). The inflammatory component represents the inflammatory changes described at MRI. White arrow =
lumen of the fistulous tract seen at MRI. (Hematoxylin-eosin stain; original magnification, 320.)

which are usually the result of necrotic lymph
nodes (8,9). The Stensen duct can be dilated
from lithiasis, stenosis, or enlarged lymph nodes
(Fig 6). At enhanced CT, the gland appears dif-
fusely hyperattenuating and may show internal
fluid collections.
At MRI, the parotid gland is variably en-
larged and heterogeneous, and the usual in-
terstitial and ductal components are poorly
visualized compared with those of a normal
gland. The gland is hypointense on T1-weighted
images and may have either higher or lower than
normal signal intensity on T2-weighted images,
depending on whether edema or cellular infil-
tration predominates (Fig 6) (5,10). If internal
abscesses are suspected, paramagnetic contrast
material may help delineate these collections.
Treatment.—Viral parotitis is managed
with nonsteroidal anti-inflammatory drugs
(NSAIDs). If bacterial parotitis is suspected,
antibiotics may be required.
Chronic Parotitis
Definition.—Chronic inflammation of the parotid
gland is most commonly caused by recurrent
infections, although other causes have been de-
scribed in the literature (17,22).
Clinical Features.—Chronic parotitis mani-
fests as facial swelling and recurrent episodes
of parotitis. Clinically, chronic inflammation
of the parotid gland most frequently mani-
fests as repeated episodes of acute sialadenitis
with associated painful swelling of the involved
gland, with intervals characterized by reduction
of symptoms and decrease of gland size (22).
Alternatively, the gland can also show (a) slowly
progressive enlargement with periodic episodes
RG • Volume 38 Number 5 Inarejos Clemente et al 7

Figure 6. Acute parotitis of the left parotid gland in a 10-year-old boy.

(a) Sagittal US image of the parotid gland shows heterogeneous paren-
chyma with multiple foci of salivary secretions (arrowheads) and lymph
nodes (*). (b) Doppler US image shows diffuse increased vascularization.
(c) Axial T2-weighted fat-suppressed MR image shows minimal dilata-
tion of the intraglandular duct (arrow) in a diffusely enlarged left parotid
gland (*). The left parotid gland parenchyma is denser than on the nor-
mal right side owing to edematous fluid and cellular infiltration.

diffusely hypoechoic with irregular margins and

small foci of calcification.

Treatment.—The acute sialadenitis event may

be managed with nonsteroidal anti-inflammatory
drugs (NSAIDs).

Chronic Sclerosing Sialadenitis

Definition.—Chronic sclerosing sialadenitis, also

of acute sialadenitis or (b) slowly progressive
painless enlargement of the salivary glands.
Epidemiology.—Recurrent parotitis is a unique
disease entity, characterized by recurrent epi-
sodes of parotitis that typically begin at 3–6 years
of age and resolve after puberty (3,10). Noninfec-
tious conditions such as irradiation, autoimmune
disease, or idiopathic causes may also lead to
chronic inflammation.
Imaging Findings.—At imaging, chronic paroti-
tis usually manifests as atrophy of the glands. At
US, there are multiple small foci of calcification
with other hypoechoic foci, which may represent
salivary secretions and small lymph nodes (Fig
7) (8,9). CT helps confirm the calcifications and
dilatation of the Stensen duct (5). At MRI, the
parotid gland shows atrophy (5) but may also
show diffuse enlargement with multiple small foci
of hyperintensity on T2-weighted images (Fig
7). As with acute parotitis, US is considered the
standard of reference. However, MRI may be in-
dicated (Fig 8), depending on the clinical evolu-
tion of the inflammatory condition.
Sometimes, chronic parotitis may be unilat-
eral, and the gland may appear atrophic and
known as Küttner tumor or chronic follicular
sialadenitis, is difficult to distinguish from other
forms of sialadenitis and shows the features of an
autoimmune process.
Clinical Features.—Chronic sclerosing sialadeni-
tis normally manifests as a painful mass of the
parotid gland secondary to chronic infection,
associated with increased inflammatory mark-
ers (23–25). Some patients may report recurrent
pain and swelling that are often associated with
food ingestion, while others may present with an
asymptomatic hard swelling of the parotid gland.
Epidemiology.—Children under 12 years old
with recurrent infections of the parotid gland are
most frequently affected, but the cause of this
inflammatory disorder is unclear (26). Sialoliths,
infectious agents, secretory dysfunctions, duct
abnormalities, and immune processes have been
proposed as causes of chronic sclerosing sialad-
enitis (6–10). It is classically described in relation
to the submandibular gland but infrequently can
also affect the parotid gland (27,28).
Imaging Findings.—At imaging, these lesions
show a well-circumscribed outline with different
8 September-October 2018 radiographics.rsna.org

Figure 7. Bilateral chronic parotitis in a 16-year-old boy. (a) Sagittal US image of the left parotid gland shows multiple
small foci of calcification (arrow) and salivary secretions (arrowheads). (b) Coronal T2-weighted MR image shows diffuse
and enlarged parotid glands containing multiple small hyperintense foci (arrowheads), which may represent salivary
secretions and lymph nodes owing to their small size. End-stage chronic parotitis will show atrophy of the glands instead.

Figure 8. Algorithm for diagnosis of suspected salivary gland inflammation.

internal features depending on the imaging
modality of choice. At US, the lesion has a cystic
appearance with internal septa (Fig 9), whereas
at enhanced CT these lesions tend to be slightly
hyperattenuating compared with the surrounding
soft tissue. At MRI, the lesion has a well-defined
nodular and solid configuration, slightly hypoin-
tense on T1-weighted images and hyperintense
on T2-weighted images (Fig 9) with intense
enhancement after contrast material adminis-
tration. Owing to the solid appearance at MRI,
internal septa are not visualized, contrasting with
the findings at US.
Histologic Findings.—Histologically, there is a
periductal and periacinar inflammation com-
pound of plasmacytic and lymphocytic infiltrate
with lymphoid follicles associated with periductal
fibrosis (Fig 9) (27).
Treatment.—Focal excision or partial paroti-
dectomy is indicated, depending on the location
RG • Volume 38 Number 5 Inarejos Clemente et al 9

Figure 9. Chronic sclerosing sialadenitis of the left parotid gland in a 12-year-old girl. (a) Transverse US image of
the parotid gland shows a well-defined nodular lesion with hypoechoic content (*) and multiple internal thick septa
(arrow). (b) On an axial T2-weighted fat-suppressed MR image, the lesion (arrow) is hyperintense and located in the
superficial lobe. (c) Sagittal oblique contrast-enhanced T1-weighted fat-suppressed MR image shows intense enhance-
ment of the lesion (arrowhead). Note the enhancement of normal parotid tissue (arrows). (d) Photograph shows super-
ficial parotidectomy of the lesion (arrow). (e) Low-power photomicrograph shows florid lymphoid hyperplasia, which
includes prominent germinal centers (*). These areas of lymphoid hyperplasia correlate with the solid appearance seen
at MRI. Note the normal parotid tissue (arrow). (Hematoxylin-eosin stain; original magnification, 330.)

of the tumor (Fig 9). Surgery can be difficult in
these cases owing to the fibrotic tissue second-
ary to the inflammatory processes. Monitoring
of the facial nerve is important to avoid damage.
Granulomatous: Mycobacterial Disease
(Tuberculosis)
Definition.—Primary tuberculous involvement
of the salivary gland is most frequently described
after systemic dissemination of pulmonary
tuberculosis.
Clinical Features.—It may manifest by mimicking
acute sialadenitis or as an insidious disease that
mimics a tumor.
Epidemiology.—It normally arises from a focus in
the tonsils or teeth, from where it spreads to the
gland via the regional lymph nodes. Sialadenitis
10 September-October 2018
Figure 10. Tuberculosis of the parotid gland in a 13-year-old boy. (a) Sagittal US image of the left parotid
gland shows a partly calcified enlarged lymph node in the parenchyma (arrow). (b) Axial contrast-enhanced T1-
weighted fat-suppressed MR image at a lower level shows peripheral enhancement of the lymph node (arrow)
with no evidence of abscess.
occurs as the infection extends from the nodes
into the gland proper (29–31).
Imaging Findings.—At cross-sectional imaging, the
findings are similar to those of bacterial parotitis.
Tuberculous involvement usually manifests as ne-
crotic nodes, which may lead to formation of focal
abscesses within the gland. In most cases, there will
be association of multiple enlarged bilateral nodes
with calcification.
At US, the intraparenchymal calcified lymph
nodes are typically seen as hypoechogenic nodules
with small foci of calcification (Fig 10) (5,8,10).
At CT, intraparotid lymph nodes show low attenu-
ation with focal calcification. At MRI, the gland
may show low-signal-intensity nodules with all
sequences (Fig 10) and sometimes formation of
abscesses (scrofula). US is considered the standard
of reference for diagnosing mycobacterial disease
of the parotid gland. However, if there is presence
of internal abscesses at US, enhanced CT will help
delineate the fluid collections for planning potential
percutaneous drainage.
Treatment.—This entity responds to the standard
treatment for mycobacterial disease.
Vascular Malformations
The new classification of the International Soci-
ety for the Study of Vascular Anomalies (ISSVA)
is based on the former classification system of
Mulliken and Glowacki (32,33) and encompasses
two different groups: vasoproliferative lesions and
vascular malformations (Table 3).
radiographics.rsna.org
Table 3: Summary of New Classifica-
tion of the International Society for the
Study of Vascular Anomalies (ISSVA)
Vasoproliferative lesions*
Infantile hemangioma
Congenital hemangioma
   Rapidly involuting congenital heman-
  gioma (RICH)
   Noninvoluting congenital hemangioma
  (NICH)
   Partially involuting congenital heman-
  gioma (PICH)
Vascular malformations†
Fast flow: arteriovenous malformation,
arteriovenous fistulas
Slow flow: capillary, venous, lymphatic, or
mixed
*Vascular tumors with increased endothelial
cell turnover.
†Congenital anomalies of the venolymphatic
system with normal endothelial cell turn-
over.
Combined Venolymphatic Malformation
Definition.—Vascular malformations are congeni-
tal anomalies of the venolymphatic system.
Clinical Features.—Venolymphatic malforma-
tions typically manifest as a sudden palpable
mass related to internal hemorrhage. If there is
association with infection, the child may show
inflammatory signs in the region.
RG • Volume 38 Number 5 Inarejos Clemente et al 11

Figure 11. Combined venolymphatic malformation involving the parotid gland in a 3-year-old girl. (a) Axial
T1-weighted MR image shows a multicystic well-defined mass involving the entire left parotid gland, with mul-
tiple hyperintense fluid-fluid levels from internal hemorrhage (arrows). (b) Axial T2-weighted MR image shows
replacement of the entire left parotid gland by the mass (arrow) with involvement of the floor of the mouth
(arrowhead). (c) Photograph of the patient shows an extensive mass in the left parotid area and the floor of the
mouth (arrow). Note the tracheostomy tube (arrowhead).

venous formations, and internal septa. Doppler

Epidemiology.—The vast majority of venolym-
phatic malformations are diagnosed in children
under 2 years of age.
According to the classification system devel-
oped by Mulliken and Glowacki (32,33), vascular
anomalies are divided into two major categories:
(a) vasoproliferative lesions (vascular tumors such
as hemangiomas), characterized by increased
endothelial cell turnover; and (b) vascular mal-
formations, characterized by normal endothe-
lial cell turnover (Table 3). The latter category
encompasses a wide range of anomalies that can
be further divided according to internal flow into
slow-flow anomalies (venous/lymphatic), fast-flow
anomalies (arteriovenous malformations and fistu-
las), and complex combined anomalies (34–36).
Imaging Findings.—At imaging, the appear-
ance may vary depending on the type of vascular
malformation, but they usually display multicys-
tic features. At US, they typically demonstrate
multicystic masses with a solid component,
interrogation will show slow flow, fast flow, or a
combination, depending on the type of vascular
malformation. CT is not routinely performed but
may show calcification or internal hemorrhage.
MRI demonstrates multilobulated and well-
defined cystic lesions, hypointense on T1-weighted
images and hyperintense on T2-weighted images
(Fig 11). If there is internal hemorrhage, some
fluid-fluid levels may be seen (Fig 11). On post-
contrast images, the lesion shows heterogeneous
enhancement in the venous phase (35). MR
angiography is the imaging modality of choice for
classification of vascular anomalies. It allows deter-
mination of extension and their anatomic relation-
ships to adjacent structures, thereby providing
important information for therapy planning.
Treatment.—Sclerotherapy with bleomycin or OK-
432 by means of direct puncture is the treatment
of choice for cystic lesions (37). This method has
shown efficacy in treatment of macrocystic lymphatic
malformations and has seldom been used in micro-
cystic lesions, where some mass reduction may be
achieved. There is currently no consensus regarding
the treatment of microcystic lymphatic malforma-
tions, although surgery is the initial approach.
Sclerotherapy causes local endothelial inflam-
mation, which tends to create adhesions between
the walls of the cysts, thus preventing further fill-
ing. The procedure is not as invasive as a surgical
procedure, and although only a partial reduction is
12 September-October 2018
to be expected, it may be repeated until the desired
loss of volume is achieved (38,39). If the lesion has
solid and cystic components, treatment is based on
a combination of sclerotherapy and surgery. Recent
studies propose sirolimus (also known as rapamy-
cin) as initial medical treatment with promising re-
sults (38). Sirolimus has a potent immunosuppres-
sant function and is especially useful in preventing
rejection of kidney transplants (38,39).
Lymphatic Malformation
(Lymphangioma)
Definition.—Lymphatic malformations are con-
genital anomalies of the lymphatic system.
Clinical Features.—Lymphatic malformations
often manifest suddenly as a palpable mass
secondary to internal hemorrhage or infection.
Other malformations are typically discovered at
prenatal US as well-defined hypoechoic masses
with internal septa (40).
Epidemiology.—The new classification of the
International Society for the Study of Vascular
Anomalies (ISSVA) classifies lymphangiomas as
lymphatic malformations (macrocystic, microcys-
tic, or mixed) (35,36). They can manifest at any
age, but 90% manifest before the age of 2 years.
Imaging Findings.—At imaging, lymphatic
malformations tend to have a cystic appearance,
unless they manifest with internal hemorrhage.
At US, these may be anechoic or hypoechoic and
show internal debris as a sign of bleeding or in-
fection. Doppler evaluation may reveal vascular-
ity in the septa. As with hemangiomas or vascular
malformations, CT is not routinely indicated for
diagnosis, but it may show fluid-fluid levels as a
sign of internal hemorrhage.
At MRI, the appearance on T1-weighted im-
ages may vary depending on the protein content
and signs of bleeding. On T2-weighted images,
these malformations usually have high signal
intensity. Fluid-fluid levels may be seen if there is
complication with hemorrhage (5,35,40). As with
vascular malformations, MRI is the most valu-
able modality for characterization of lymphatic
malformations.
Histologic Findings.—Lymphatic malformations
can be circumscribed microcystic and macrocys-
tic lesions. They are composed of interconnected
lymphatic channels dilated by variable amounts
of smooth muscle in the wall of the vessel. The
vessels are lined by flat endothelial cells, which
are positive for D2-40. The vessels are usually
surrounded by lymphoid tissue.
radiographics.rsna.org
Treatment.—The treatment depends on the ap-
pearance at MRI. If the lesion is composed of large
cysts (macrocystic lesion), the initial treatment is
sclerotherapy with different agents (doxycycline,
bleomycin, OK-432) (38), surgery, or a combina-
tion of both. If the lesion is microcystic, consensus
has not been reached about the treatment and it
is more controversial. Some authors use the same
sclerosing agents, while others opt to remove the
lymphatic malformation. If there is obstruction of
the airway or potential cosmetic malformation, the
lesion is surgically excised early on.
Recent genetic studies have discovered an
association of the mTOR (mammalian target of
rapamycin) gene with some lymphatic malfor-
mations (39). If the tumor cells express this pro-
tein on the surface membrane, they are sensitive
to rapamycin.
Neoplastic Lesions
Parotid gland tumors are rare in the pediatric
population but comprise a wide range of patho-
logic diagnoses, most of them benign (3,4). This
combination makes diagnosis and treatment
challenging, especially in children. However, if
clinically there is suspicion of a parotid gland
mass, the initial workup differs from that of the
approach to infection (Fig 12).
Benign Tumors
Pleomorphic Adenoma
Definition.—Pleomorphic adenomas are also
known as benign mixed tumors and have an
epithelial origin.
Clinical Features.—Pleomorphic adenomas
typically manifest as slow-growing, painless,
firm masses with an average interval from onset
of signs and symptoms to initial workup of 1–3
years (1,3,4,41).
Epidemiology.—These tumors affect patients
from 1 to 20 years of age and are the second
most common neoplasm of the parotid gland af-
ter hemangioma, representing 40% of all benign
parotid tumors (41). Pleomorphic adenomas
account for approximately half of all epithelial
tumors of the salivary glands and more than 90%
of benign salivary gland epithelial tumors (3,4).
Imaging Findings.—At imaging, pleomorphic ad-
enomas are seen as a benign-appearing mass and
typically manifest as well-defined encapsulated
masses. Dystrophic calcifications can occasionally
be seen scattered throughout the tumor; such cal-
cifications are highly characteristic of this diagno-
RG • Volume 38 Number 5
Figure 12. Algorithm for diagnosis of a suspected solid mass or neoplasm of the parotid gland. Chemo = chemotherapy,
RT = radiation therapy.
sis. Larger lesions are more heterogeneous owing
to necrosis or hemorrhage, findings normally not
present in smaller lesions. At US, pleomorphic
adenomas tend to be hypoechoic to isoechoic
compared with the rest of the parotid gland and
may show small foci of calcification (Fig 13).
At CT, most small benign mixed tumors are
smoothly marginated and well encapsulated,
with lower attenuation than the surrounding
parotid parenchyma. At MRI, they manifest as
well-defined masses with low signal intensity on
T1-weighted images, high signal intensity on
T2-weighted images, and a variable degree of
enhancement (Fig 13). A low-signal-intensity
capsule is often seen on T2-weighted images and
fat-suppressed images (Fig 13) (5,11,12,42).
MRI is considered the standard of reference for
imaging pleomorphic adenoma, as it clearly de-
marcates borders along with soft-tissue extension
and perineural invasion.
When a lobulated well-defined mass has cen-
tral necrosis, pleomorphic adenoma should be
considered in the differential diagnosis.
Histologic Findings.—Pleomorphic adenoma is
a well-circumscribed tumor consisting of epithe-
lial compound and fibromyxoid stroma, which
is why it is also called biphasic tumor. Most of
the epithelial component is glandular with foci of
Inarejos Clemente et al 13
squamous metaplasia (43). This glandular com-
ponent is lined by myoepithelial cells, which may
be cuboidal, flattened, or spindle shaped. The
stromal component may be fibromyxoid with
often cartilaginous differentiation (44). Hemor-
rhage, necrosis, calcification, or hyalinization may
be present in the stromal component.
Treatment.—Superficial parotidectomy, selective
deep lobe parotidectomy, or total parotidectomy
is indicated for pleomorphic adenoma, depend-
ing on the location of the lesion (Fig 13). The
risk of tumor recurrence after lesion enucleation
approaches 43% (41). The traditional incision
to the parotid gland is the “lazy S” described by
Blair (45), which provides good surgical exposure
but produces a visible scar. Appiani (46) modi-
fied the face-lift incision to achieve better cos-
metic results, and in certain patients this incision
can be reduced in its retroauricular extension by
performing a partial face-lift approach.
Subcutaneous and superficial musculoaponeu-
rotic system (SMAS) flaps are used to recon-
struct the postoperative preauricular defect and
reduce the incidence of Frey syndrome, a late
complication of parotid surgery that may develop
in some patients. Identification and dissection
of the facial trunk and branches is mandatory,
and monitoring is helpful to avoid damaging
14 September-October 2018 radiographics.rsna.org

Figure 13. Pleomorphic adenoma of the left parotid gland in a 15-year-old girl. (a) Sagittal US image of the
left parotid gland shows a multilobulated well-defined hyperechoic mass (arrow). Note the normal parotid gland
tissue (*). (b) Axial T2-weighted MR image shows the typical low-signal-intensity capsule (arrow). (c) Coronal
contrast-enhanced T1-weighted fat-suppressed MR image shows heterogeneous peripheral enhancement of the
lesion (arrow) with internal necrosis (*). (d) Photograph from superficial parotidectomy shows a mass lined by a
capsule (*) and the facial trunk nerve (arrow).

the nerve. Superficial parotidectomy preserving
the facial nerve is the standard of reference, but
when the tumor is located in the deep lobe, total
parotidectomy must be performed. Damage to
the auriculotemporal nerve during surgery leads
to sweating and flushing of the face when eating
or thinking about food.
Dermoid Cyst
Definition.—Dermoid cysts can be congenital
or acquired. Congenital cysts arise from a rest of
embryonic epithelium, while acquired cysts are the
result of traumatic implanted skin in deeper layers.
Clinical Features.—Dermoid cysts are usually
slow-growing painless masses that elevate the skin
and often have a central punctum, which rep-
resents the plugged orifice of the pilosebaceous
follicle (47).
Epidemiology.—Dermoid cysts account for less
than 10% of parotid tumors (48,49).
Imaging Findings.—At imaging, dermoid cysts
are ovoid with a smooth and noninfiltrating rim,
which favors a benign nature. The superficial
margin of the cyst usually extends to the deep
skin line, and the cyst is filled with mucoid atten-
uation material and scattered dystrophic calcifi-
cations. At US, they may have a solid appearance
owing to the mucoid component.
At CT, they may show different attenuations
depending on the content, which could be fluid, fat,
or soft tissue. At MRI, cysts that contain fat appear
hyperintense on T1-weighted and T2-weighted im-
ages, whereas if they contain fluid, they are hypoin-
tense on T1-weighted images and hyperintense on
T2-weighted images. They may also demonstrate
soft-tissue signal intensity (Fig 14) (47).
Histologic Findings.—Pathologic examination
demonstrates squamous epithelium lining the
cyst wall. The fibrocollagenous cyst wall con-
tains mature adnexal structures such as hair
follicles and sebaceous, eccrine, and apocrine
glands (Fig 14).
RG • Volume 38 Number 5 Inarejos Clemente et al 15

Figure 14. Dermoid cyst involving the right parotid gland in a 9-year-old patient. (a) Axial T1-weighted MR
image shows a nodular lesion in the superficial lobe. The lesion has low internal signal intensity (arrow) owing to
the presence of fluid. (b) Axial T2-weighted MR image shows a hyperintense well-defined nodule (arrow) with
internal fluid (*). Note the heterogeneity of the high-signal-intensity fluid due to the presence of protein con-
tent. (c) Low-power photomicrograph shows keratinizing squamous epithelium with pilosebaceous structures
in the wall of the cyst (*). Note the protein content (arrowheads). The area of fluid with protein content in b
corresponds to the lumen of the cyst. (Hematoxylin-eosin stain; original magnification, 320.)

Epidemiology.—Infantile hemangioma is the most

prevalent benign tumor of the parotid gland, ac-
counting for 90% of salivary gland lesions that oc-
cur in children before 1 year of age. These tumors
are composed of vascular endothelium, which
undergoes a rapid growth phase followed by a slow
spontaneous involution, which occurs gradually
over several years and is generally complete by
the end of the 1st decade. Approximately 20% of
hemangiomas are present at birth, with the rest
arising shortly thereafter (35,50).

Imaging Findings.—All imaging modalities

Treatment.—Dermoid cysts must be entirely
excised to avoid recurrence. Superficial paroti-
dectomy with preservation of the facial nerve
for treatment of parotid dermoid cyst has been
reported in the literature (49).
Infantile Hemangioma
Definition.—Infantile hemangioma is the most
common benign vascular tumor in the pediatric
population (35).
Clinical Features.—Infantile hemangiomas
manifest as a unilateral soft-tissue mass at the
level of the parotid region, with or without blu-
ish discoloration of the skin. Results of clinical
examination at birth are normal in the majority
of hemangiomas, since they usually appear 1 or 2
months after birth.
show a lobulated solid hypervascular mass. At
US, the affected parotid gland appears diffusely
enlarged with intense vascularization at Doppler
examination (Fig 15). CT is not indicated if an
infantile hemangioma is suspected, but if CT
is performed, it usually shows intense enhance-
ment in the arterial phase. At MRI, the parotid
gland is diffusely enlarged with lobulated mar-
gins, appearing homogeneously hypointense on
T1-weighted images and homogeneously hyper-
intense on T2-weighted images, with intense en-
hancement in the arterial phase (Fig 15) (5,35).
The diagnosis is made clinically in most cases.
Doppler US is the modality of choice, although
MRI may be useful in clinically difficult cases,
when there is normal overlying skin, when evalua-
tion of extension is necessary, for guiding therapy,
and for evaluating response to treatment.
Histologic Findings.—Infantile hemangiomas
have a focal nodular growth pattern or plaque-like
16 September-October 2018 radiographics.rsna.org

Figure 15. Right parotid hemangioma in a 2-week-old girl. (a) Left: Transverse US image shows a heterogeneous and
enlarged parotid gland with thick internal septa (arrow) in the right parotid region. Right: Transverse US image shows a
normal left parotid gland (*). (b) Axial T2-weighted MR image shows a diffusely enlarged parotid gland with lobulated
margins that is homogeneously hyperintense (arrow); it was homogeneously hypointense on T1-weighted images (not
shown). There are no signs of infiltration into the adjacent soft tissue. (c) Coronal MR angiogram in the arterial phase
shows homogeneously intense enhancement of the gland (arrow). (d) Clinical photograph shows a large swelling in
the anatomic area of the right parotid gland (arrow). (e) Clinical photograph at 9 months of age shows that progressive
spontaneous involution of the hemangioma has occurred, with no clinical evidence of a mass.

pattern. They show a histologic spectrum of lobu-
larity and cellularity depending on the evolution-
ary phase. The proliferative phase shows densely
cellular lobules of capillaries lined by plump en-
dothelial cells with mitotic figures. In the involu-
tional phase, there are dilated capillary structures
with flattened endothelial cells and fibrous tissue.
Glucose transporter 1 (GLUT 1) is a marker for
infantile hemangioma.
Treatment.—Treatment is not required because
infantile hemangiomas normally involute (Fig 15).
RG • Volume 38 Number 5 Inarejos Clemente et al 17

Figure 16. Neurofibroma involving the parotid gland. (a) Axial T2-weighted MR image at 7 months
of age shows a heterogeneous and enlarged right parotid gland (arrow). The mass is heterogeneously
hyperintense; it was heterogeneously hypointense on T1-weighted images (not shown). (b) Axial T2-
weighted fat-suppressed MR image at 4 years of age shows increased size of the right parotid neuro-
fibroma (arrow) despite medical treatment. Note the complete replacement of the parotid gland by
the neurofibroma.

The lesion is systemically treated only when it is
complicated by ulceration/infection, causes com-
pression of the airway, or is in a location where it
can lead to a cosmetic malformation in the future.
Recent treatments include oral propranolol (51,52).
Neurogenic Tumors: Neurofibroma
There are five main tumor types that may arise
from the nerve sheath: neurofibroma, schwan-
noma, malignant peripheral nerve sheath tumor,
neuroma, and perineurioma. Neurofibroma is
the most common tumor of the peripheral nerve
sheath tumor group. They tend to be solitary, and
up to 90% are seen in patients without neurofi-
bromatosis type 1.
Definition.—Neurofibromas may consist of
solitary or multiple benign tumors, which are
sharply delineated and arise primarily from
the nerve sheath of the facial nerve trunk or its
branches (53).
Clinical Features.—While the manifestations vary
depending on the location of the tumor, neurofi-
bromas often manifest as a slow-growing painless
mass in the cervical and periparotid regions.
heterogeneous echotexture, with several areas
displaying the characteristic appearance of central
hyperechogenicity, peripheral hypoechogenicity,
and areas of shadowing. At CT, neurofibromas
tend to be homogeneously cystic or isoattenuat-
ing to muscle with moderate enhancement after
contrast material administration.
At MRI, neurofibromas are of low to interme-
diate signal intensity on T1-weighted images and
hyperintense on T2-weighted images and may
show the “target sign” (11). They may contain
ill-defined areas of heterogeneous signal intensity,
which complicates differentiation from pleomor-
phic adenoma. MRI is the standard of reference
for defining extension of the lesion and involve-
ment of the adjacent soft tissue (Fig 16).
Histologic Findings.—Neurofibromas are
composed of Schwann cells, fibroblasts, and
perineurium-like cells. These cells usually have
elongated or wavy nuclei and inconspicuous
cytoplasm, scattered in a myxoid stroma. Tumor
cells are small and round or oval, with clumped
chromatin and minimal cytoplasm. Rosettes are
frequently found, and mitoses vary from moder-
ate to numerous.

Epidemiology.—There is a strong association with Treatment.—The vast majority of neurofibro-

neurofibromatosis (type 1), and when this condi-
tion is present, neurofibromas are multiple (54).
Imaging Findings.—Neurofibromas are well-de-
fined nonencapsulated solid masses that infiltrate
between the nerve fascicles. At US, they have
mas do not need treatment. They should be
treated if they are symptomatic, show rapid
growth, involve the airway, or may lead to a
cosmetic anomaly in the future. The treatment
of choice for plexiform neurofibromas is surgical
resection, but if surgery cannot remove at least
18 September-October 2018
80% of the mass, these may be treated medi-
cally. Currently, experimental treatments such
as trametinib or selumetinib are being used, but
they remain controversial (55).
Malignant Tumors
Malignant tumors of the parotid gland represent
approximately 35% of salivary gland tumors in
children (3,4,12), with mucoepidermoid carci-
noma being the most frequent (3). Mucoepider-
moid carcinoma is by far the most common type
of malignant salivary gland tumor in children, ac-
counting for more than 60% of cases (3). Acinic
cell carcinoma (11%), adenocarcinoma (10%),
and adenoid cystic carcinoma (9%) are the three
next most common.
Mucoepidermoid Carcinoma
Definition.—Mucoepidermoid carcinoma is the
most common malignant salivary gland tumor
in children.
Clinical Features.—Mucoepidermoid carcinoma
tends to manifest as a firm, slow-growing, painless
mass in the parotid gland. At clinical examination,
the facial nerve is usually preserved and no inflam-
matory markers are associated (56,57). The average
time before the patient first experiences symptoms
of the tumor is around 8–12 months (57,58).
Epidemiology.—Mucoepidermoid carcinoma
is most commonly reported in the middle-aged
group (35–65 years of age), but it is the most
frequent malignant salivary gland neoplasm
in patients under 20 years of age, with a slight
predilection for females (58,59). Radiation
exposure is one of the most prevalent etiologic
triggers (60,61).
Imaging Findings.—The radiologic appearance
usually depends on the grade of the tumor. At
US, mucoepidermoid carcinoma is a well-cir-
cumscribed hypoechoic lesion with a partial or
completely cystic appearance. At CT, high-grade
tumors usually have cystic areas, being more
heterogeneous in appearance than low-grade
lesions. MRI allows detailed soft-tissue charac-
terization of the tumor and provides important
information about tumor margins, extent and
depth of the lesion, pattern of tumoral infiltra-
tion into the adjacent parenchyma, and presence
of perineural spread (11,12).
Low-grade tumors have a benign appearance,
with well-defined and smooth margins. Cystic
areas are frequently described, but calcification
is less common than in other tumors. These
findings are similar to those of a benign mixed
radiographics.rsna.org
tumor. MRI features are also indistinguish-
able from those of pleomorphic adenoma. At
MRI, low-grade mucoepidermoid carcinoma
can mimic other solid benign tumors, such as
pleomorphic adenoma, and therefore is often
considered in the differential diagnosis (Fig 17).
In contrast, high-grade tumors have ill-
defined margins with an infiltrating appearance.
At MRI, high-grade carcinomas tend to have
low to intermediate signal intensity on both
T1-weighted and T2-weighted images, poorly
defined margins with infiltration into the para-
pharyngeal space and surrounding musculature,
and heterogeneous enhancement after contrast
material administration (11). At MRI, there
are no pathognomonic findings to characterize
mucoepidermoid carcinoma. MRI is superior
in defining tumor characteristics and extension,
particularly perineural spread. The presence of a
solid component with internal necrosis indicates
the need for a biopsy.
Histologic Findings.—Mucoepidermoid carci-
noma is classified histologically as low, interme-
diate, and high grade on the basis of the relative
proportions of cell types. The histologic pattern
consists of a combination of squamous and
mucous, intermediate, and clear cells arranged
in cords, sheets, or cystic configurations (62,63).
Well-differentiated or low-grade tumors are
predominantly composed of mucinous cells, but
high-grade mucoepidermoid carcinoma shows a
solid and infiltrative pattern (64).
Treatment.—For low-grade carcinomas, the
treatment of choice is complete surgical resec-
tion, but for high-grade carcinomas or tumors
with deep lobe involvement, children may un-
dergo a parotidectomy with lymph node dissec-
tion of the neck (Fig 17) (65,66).
The surgical approach is the same as in be-
nign tumors, and the goal is surgical resection of
the mass with clear margins, including the sur-
rounding tissues of the parotid gland in case of
proximity. The facial nerve must be preserved as
much as possible. Tumor recurrence is reported
in 7%–20% of patients (66). Local recurrence
is more likely to occur in patients with positive
surgical margins, regardless of tumor grade.
Lymphoma
Definition.—Owing to their origin in the mucosal
lymphoid tissue, primary lymphomas of the pa-
rotid gland are classified as MALT (mucosa-asso-
ciated lymphoid tissue) lymphomas (MALToma),
and these account for 4.7% of lymphomas from
all sites of the body (67).
RG • Volume 38 Number 5 Inarejos Clemente et al 19

Figure 17. Mucoepidermoid carcinoma involving the superficial lobule of the right parotid gland in a 16-year-old boy.
(a) Axial T1-weighted MR image shows a hypointense mass with irregular margins (*) and no evidence of a clear plane
of separation from the normal parotid parenchyma. (b) Axial contrast-enhanced T1-weighted fat-suppressed MR image
shows heterogeneous enhancement of the mass due to necrosis (arrow). Note the ill-defined margins, which make it
difficult to delineate. (c) Photograph shows right total parotidectomy (*) with preservation of the facial nerve. Blue ves-
sel loop indicates the temporofacial (arrowhead) and cervicofacial (arrow) branches of the facial nerve. (d) Low-power
photomicrograph shows a low-grade tumor predominantly composed of squamous cells (arrows) and mucinous cells
(*) with no evidence of mitoses. The internal necrosis seen at MRI after contrast material administration is due to the
mucinous cell component. (Hematoxylin-eosin stain; original magnification, 330.)

Clinical Features.—Lymphoma of the parotid T2-weighted images, with uniform enhancement

gland often manifests as a painless progressively
enlarging mass that is rarely suspected before
biopsy or surgical removal. It can manifest as fo-
cal or diffuse, single or multiple, and unilateral or
bilateral masses (67,68).
Epidemiology.—Primary lymphoma of the pa-
rotid gland is a rare condition, described in up to
80% of the reported cases in the literature (1).
Imaging Findings.—At cross-sectional imaging,
the appearance of lymphoma is highly variable,
manifesting as focal or diffuse, single or multiple,
and unilateral or bilateral masses. At enhanced
CT, the gland is diffusely enlarged with a variable
degree of enhancement. At MRI, primary lym-
phoma of the parotid gland usually has homoge-
neous intermediate signal intensity on T1- and
of the gland on postcontrast images.
Associated cervical lymphadenopathy will be
evident at MR imaging (Fig 18) (5). Enhanced
CT of the neck will also allow detection of en-
larged lymph nodes in other regions. The associa-
tion with lymphadenopathy in other regions of the
neck requires biopsy of the enlarged parotid gland.
Histologic Findings.—The large majority of
lymphomas in the parotid gland are of the
MALT type. These neoplasms derive from B cells
associated with epithelial tissue. They may be
composed of either large cells or small cells. The
pattern can be diffuse or nodular. MALT lym-
phomas characteristically show infiltrates of small
centrocytes and monocytoid B cells with variable
plasma cell differentiation, which invade parotid
ductal and acinar tissue (68).
20 September-October 2018
Figure 18. Lymphoma involving the parotid gland in a 12-year-old girl. (a) Axial T2-weighted fat-sup-
pressed MR image shows an enlarged left parotid gland with homogeneous intermediate signal intensity
(arrow). Note the enlarged lymph nodes in the laterocervical region bilaterally (arrowheads). (b) Axial
contrast-enhanced T1-weighted fat-suppressed MR image at a lower level shows lymphadenopathy in
the neck bilaterally (arrows).
These lymphomas usually contain a lympho-
epithelial component associated with a nonneo-
plastic area with prominent germinal centers. The
malignant cells are characterized by immunore-
activity for CD19, CD20, and surface immuno-
globulins. Cytogenetically, the t(11;14) trans-
location is present in about 70% of cases. This
lymphoma may be difficult to distinguish from
follicular hyperplasia. Assessment of the clonal-
ity of the cells with immunohistochemistry is an
important tool for confirming the diagnosis.
Treatment.—Treatment of lymphoma consists
of chemotherapy, usually with a regimen of four
drugs known as CHOP (cyclophosphamide,
doxorubicin, vincristine, and prednisone) plus
the monoclonal antibody rituximab (Rituxan;
Genentech, South San Francisco, Calif).
Rhabdomyosarcoma
Definition.—Rhabdomyosarcoma of the parotid
gland is a malignant tumor that can be histologi-
cally classified into three types: alveolar, embryo-
nal, and pleomorphic (or adult type).
Clinical Features.—The clinical features depend
on the location of the tumor, but rhabdomyo-
sarcomas of the parotid gland generally manifest
as swelling at the angle of the mandible, rapidly
increasing in size (69,70). Pain and facial pa-
ralysis are common at presentation (24%) (71),
reflecting the aggressive nature of the tumor and
its degree of extension.
Epidemiology.—Rhabdomyosarcoma is consid-
ered the most common soft-tissue sarcoma in the
radiographics.rsna.org
pediatric population and the seventh most com-
mon malignancy in children overall (4%–8% of
cases) after leukemia, central nervous system tu-
mors, lymphoma, neuroblastoma, Wilms tumor,
and bone cancer (69–71). This tumor manifests
at a younger age than other malignant salivary
gland neoplasms, with 70% occurring between
the ages of 1 and 8 years (70).
A large proportion of rhabdomyosarcomas
occur in the head and neck (40%). Embryonal
rhabdomyosarcoma is the most common subtype
that may secondarily invade the parotid gland.
The alveolar type normally arises in the extremi-
ties and trunk and has the worst prognosis.
Imaging Findings.—At cross-sectional imaging,
rhabdomyosarcoma is markedly heterogeneous
with internal areas of necrosis. Intratumoral
hemorrhage is uncommon, and calcification is
typically absent. At enhanced CT, the tumor is
heterogeneously isoattenuating with ill-defined
low-attenuation areas due to necrosis.
At MRI, the tumor is isointense to muscle
on T1-weighted images and hyperintense on
T2-weighted images with different patterns of
enhancement, depending on the presence of
necrosis (5,11,72,73). It demonstrates irregular
margins and may involve adjacent soft tissues and
bony structures by direct infiltration (Fig 19).
MRI is essential to define extension and infiltra-
tion of adjacent soft tissue and the carotid space.
The presence of a solid component with internal
necrosis indicates the need for biopsy.
Histologic Findings.—Rhabdomyosarcoma is typi-
cally composed of loose myxoid to densely cellular
undifferentiated cells. Myogenin and MyoD1
RG • Volume 38 Number 5
Figure 19. Rhabdomyosarcoma involving the parotid gland in a 9-year-old girl. (a) Axial T1-weighted MR
image shows a heterogeneous isointense mass (*) in the right parotid gland. Note the direct involvement of
the retromandibular vein (arrow). (b) Axial T2-weighted MR image after chemotherapy shows a heterogeneous
right parotid gland (arrow) with no evidence of tumor.
stains are positive in tumoral cells of embryonal
and alveolar rhabdomyosarcoma (74,75). Genetic
features of alveolar rhabdomyosarcoma are char-
acterized by fusion of the FOXO1 gene with either
the PAX3 or PAX7 gene.
Treatment.—Treatment consists of chemother-
apy in accordance with the Memorial Sloan-Ket-
tering Cancer Center (MSKCC) protocol and
adjuvant radiation therapy. The MSKCC proto-
col for high-risk rhabdomyosarcomas is based on
vinca alkaloids, alkylating agents, and topoisom-
erase II inhibitors, with a window of maintenance
phase with irinotecan and carboplatin. Surgery
is usually dismissed owing to the high morbidity
associated with the procedure. Local control is
routinely achieved with photon radiation therapy
focused on the primary tumor and laterocervical
lymph node chain.
Conclusion
Knowledge of the normal anatomy of the pa-
rotid gland region and its appearance at different
cross-sectional imaging modalities in children is
crucial for avoiding diagnostic pitfalls and recog-
nizing normal variants. Cross-sectional imaging is
essential to characterize congenital, inflammatory,
vascular, and neoplastic processes and select the
appropriate treatment course (Tables 4, 5) while
avoiding unnecessary or aggressive diagnostic
procedures or therapy.
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22 September-October 2018 radiographics.rsna.org

Table 4: Nonneoplastic Differential Diagnoses for Parotid Gland Lesions in Children

Physical Examination
Differential Diagnosis Results/Symptoms Radiologic Key Features Treatment
Congenital
First branchial cleft Recurrent tender mass in Well-defined tubular or Surgical resection of cyst
cysts preauricular region ap- rounded cystic lesions that and/or fistula, including
pearing after infection of may extend to skin (fistula) sinus track
upper respiratory tract
Inflammatory
Acute parotitis Swelling and tenderness of Enlargement of parotid gland Viral: NSAIDs*
parotid region with or with multiple lymph nodes Bacterial: NSAIDs* with
without fever or without antibiotics
Chronic parotitis Recurrent episodes of acute Atrophy of gland with calcifi- NSAIDs* for acute event
sialadenitis with intervals cations and small lymph of sialadenitis
without any symptoms nodes
Chronic sclerosing Painful mass in parotid US: well-defined nodule Focal excision or partial
sialadenitis gland due to chronic with cystic appearance and parotidectomy
infection internal septa
CT/MRI: well-defined nod-
ule with solid appearance
Tuberculosis Symptoms may suggest Necrotic and partly calcified Drugs for mycobacterial
acute infection or slow- parotid lymph nodes disease
growing tumor
Vascular
Combined venolym- Palpable mass due to inter- Multicystic mass with one or Sclerotherapy with bleo-
phatic malformation nal hemorrhage more solid components, mycin or OK-432
venous formations, and
internal septa with or with-
out fluid-fluid levels due to
hemorrhage
Lymphatic malforma- Palpable mass due to inter- Well-defined cystic mass with Sclerotherapy with
tion nal hemorrhage or without fluid-fluid levels bleomycin or OK-432,
Prenatal diagnosis due to hemorrhage surgery, or a combina-
tion of both
*NSAID = nonsteroidal anti-inflammatory drug.

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RG • Volume 38 Number 5 Inarejos Clemente et al 23

Table 5: Neoplastic Differential Diagnoses for Parotid Gland Lesions in Children

Physical Examination Re-

Differential Diagnosis sults/Symptoms Radiologic Key Features Treatment
Benign tumors
Pleomorphic adenoma Slow-growing (1–3 years), Well-defined encapsulated Superficial parotidectomy,
painless, firm mass mass selective deep lobe
At MRI, low-signal-intensity parotidectomy, or total
capsule is often seen on parotidectomy, depend-
T2-weighted images ing on location of lesion
Dermoid cyst Slow-growing painless Well-defined ovoid nodule Focal excision to avoid
nodule with central that may contain fluid, fat, recurrence
punctum or soft tissue
Infantile hemangioma Symptoms usually appear Lobulated, solid, hypervascu- Not required, as these
1 or 2 months after birth lar mass hemangiomas usually
spontaneously involute
Neurofibroma Slow-growing painless Nonencapsulated well- Not required
mass defined solid masses with
“target sign”
Malignant tumors
Mucoepidermoid Firm, slow-growing, pain- Low-grade tumors: partial or Low-grade tumors: com-
carcinoma less mass complete cystic appearance plete surgical resection
High-grade tumors: solid High-grade tumors: paroti-
appearance with internal dectomy with dissection
necrosis of cervical lymph nodes
Lymphoma Painless progressive Gland is diffusely enlarged CHOP* plus rituximab
enlargement of parotid with variable degree of
gland enhancement in association
with cervical lymphade-
nopathy
Rhabdomyosarcoma Swelling and pain at angle Large heterogeneous mass Chemotherapy and adju-
of mandible with rapid with internal necrosis with vant radiation therapy
increase in size with or or without invasion of adja-
without facial paralysis cent soft tissue
*CHOP = cyclophosphamide, doxorubicin, vincristine, and prednisone.

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