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An Algorithm Approach to Diagnosing Bilateral Parotid Enlargement

Si Chen, Benjamin C. Paul and David Myssiorek
Otolaryngology -- Head and Neck Surgery 2013 148: 732 originally published online 4 February 2013
DOI: 10.1177/0194599813476669

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State of the Art Review
An Algorithm Approach to
Diagnosing Bilateral Parotid
Enlargement
Si Chen, MD1, Benjamin C. Paul, MD1, and
David Myssiorek, MD1
No sponsorships or competing interests have been disclosed for this article.
Abstract
Objective. This contemporary review aims to categorize the
disease entities that cause bilateral parotid enlargement and
to develop a question-based algorithm to improve diagnosis
of bilateral parotid masses.
Data Sources. A PubMed search for bilateral and parotid
showed 818 results. Of these, 68 relevant studies were
reviewed to compile a list of disease processes that can
cause bilateral parotid enlargement.
Review Methods. A total of 22 diseases entities were
reviewed. The disease processes were initially grouped into
6 categories based on etiology: sialadenosis, infection, neo-
plasm, autoimmune, iatrogenic, and miscellaneous. For each
lesion, the incidence, history, and physical examination were
compiled in a matrix.
Conclusion. After reviewing the matrix, it was clear that
grouping diseases based on specific history and physical find-
ings limits the differential diagnosis. The most important fac-
tors included disease incidence, timing of onset, nodular or
diffuse, pain, and overlying skin changes. With this algorithm,
the differential diagnosis can be limited from 28 to 7 or
fewer likely diagnoses for a given presentation.
Implications for Practice. Bilateral parotid disease has a wide
differential diagnosis with an expanding number of available
tests. An algorithm, based solely on data obtained from the
history and physical examination in the first patient encoun-
ter, may reduce the differential and aid the clinician in decid-
ing on further workup and treatment. Following the
algorithm presented here should allow the clinician to arrive
at a diagnosis rapidly without ordering unnecessary tests
and wasting resources.
Keywords
bilateral parotid enlargement, algorithm
Received August 12, 2012; revised December 24, 2012; accepted
January 10, 2013.
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Otolaryngology
Head and Neck Surgery
148(5) 732739
American Academy of
OtolaryngologyHead and Neck
Surgery Foundation 2013
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0194599813476669
http://otojournal.org
A
lthough not as common as unilateral parotid enlar-
gement, bilateral parotid gland enlargement has a
wide differential diagnosis, which encompasses
infectious, neoplastic, autoimmune, metabolic, and iatro-
genic etiologies. In 2002, Mandel and Surattanont1 reviewed
19 disease entities with bilateral parotid enlargement. Since
then, the body of knowledge has grown due to the advances
in molecular cell technology and imaging studies. During
the review, studies have surfaced that questioned the way
we viewed certain disease entities. Most of the disease enti-
ties have not changed, but some are making a comeback,
such as viral mumps.2-4 The research efforts to understand
the pathophysiology of the diseases have better enabled us
to differentiate one diagnosis from another and definitely
confirm diagnosis. For example, the subcategorization of
lymphoepithelial lesions in human immunodeficiency virus
(HIV)positive patients continuous to improve.5 New stud-
ies have shed light on sialadenosis in diabetic and cirrhotic
patients, increasing our awareness of the insidious impact of
these diseases.6,7 Rare cases, such as Kimura disease, are
reported at an increasing rate, allowing better characteriza-
tion of symptoms and pathological processes.
One decade after the review by Mandel and Surattanont,1
we examined new and old data to formulate an algorithm
that quickly narrows the differential diagnosis of bilateral
parotid enlargement.
Algorithm Construction
A literature search using MeSH terms on PubMed, including
bilateral and parotid, revealed 818 studies. From this list,
68 articles relevant to bilateral parotid enlargement were
selected. Twenty-four major disease processes were identi-
fied, and the relevant history and physical exam findings
1
Department of OtolaryngologyHead and Neck Surgery, New York
University School of Medicine, New York, New York, USA
This article was presented at the Triological Society Combined Section
Meeting; January 26-28, 2012; Miami, Florida.
Corresponding Author:
David Myssiorek, MD, Department of Otolaryngology, New York University
Clinical Cancer Center, 160 East 34th St, 9th Floor, New York, NY 10016,
USA
Email: david.myssiorek@nyumc.org
Chen et al 733

Table 1. Matrix of Differential Diagnoses of Bilateral Parotid Enlargement with (1) or without () Specific History and Physical Findings
Diagnosis Rapid Onset Pain Nodular Firm Overlying Skin Changes

Sialadenosis
Bulimia nervosa/anorexia nervosa 2 2 2 2 2
Alcoholism/cirrhosis 2 2 2 2 2
Malnutrition 2 2 2 2 2
Endocrine 2 2 2 2 2
Infectious
Viralmumps 1 1 2 1 1
ViralHIV (BLEC/DILS) 2 2 1 2 2
Acute suppurative parotitis 1 1 2 1 1
Tuberculosis 2 1/ 1/ 1 1/
Bilateral abscess 1 1 1 1 1
Neoplastic
Warthin tumor 2 2 1 1/ 2
MALT lymphoma 1 2 1/ 1 2
Oncocytomas 2 2 1/ 1 2
Autoimmune
Recurrent parotitischild 1 1 2 1 2
Recurrent parotitisadult 2 1/ 2 1 2
Sjogrens syndrome 2 1/ 2 1 2
Wegeners granulomatosis 1 1/ 2 1 2
Sarcoidosis 1/ 1/ 2 1 1
Iatrogenic
General anesthesia 1 2 2 1/ 2
Iodide mumps 1 1 2 2 2
Radioiodine therapy 1/ 1/ 2 2 1
Kimura disease 2 2 2 1 1
Miscellaneous
Polycystic parotid disease 2 2 1 1/ 2
Amyloidosis 2 2 2 1 2
Pneumoparotitis 1 1/ 2 1/ 1
Abbreviations: BLEC, benign lymphoepithelial cyst; DILS, diffuse infiltrative lymphocytosis syndrome; HIV, human immunodeficiency virus; MALT, mucosa-asso-
ciated lymphoid tissue.

each of these diseases were collected. A matrix was built
based on consistently reported disease characteristics, includ-
ing disease incidence, bilaterality, timing of onset, nodularity,
pain, and presenting skin changes (Table 1). It should be
noted that additional signs and symptoms, including facial
nerve status, associated otalgia, and systemic symptoms,
were considered although not included as the reported data
are incomplete.
Next, an algorithm was constructed to narrow the diagno-
sis via permutation and factoring analysis. To make the
algorithm most clinically relevant, history-based signs and
symptoms served as initial branch points followed by signs
identified on physical examination as this parallels the clini-
cal workup. When reviewing the options with which to
build the algorithm matrix (Table 1), various grouping stra-
tegies were tested with a goal of using the fewest branches
to limit final subgroups. After testing the permutations with
a goal of keeping history before physical exam in the final
algorithm, the most efficient way to approach bilateral
parotid enlargement was to first narrow the differential diag-
nosis first by timing of disease onset, followed by pain,
both key pieces of information obtained from the history of
a patients disease. Last, the clinician may further hone the
diagnosis based on nodularity of the lesions palpated during
physical exam. Our algorithm is presented in Figure 1.
Ultimately, the goal of this algorithm is to help the clinician
limit the differential diagnosis on the first clinic visit of a
patient presenting with bilateral parotid enlargement, before
further laboratory or radiographic data are obtained.
It is important to keep in mind whether the suspected dis-
ease entity is more likely to present with bilateral or unilat-
eral parotid enlargement. The approximate percentage of
bilateral involvement in parotid enlargement is demon-
strated in Figure 2.
It is important to recognize that this algorithm is based
on the most common diseases and presentations of bilateral
parotid enlargement. There may be situations of combined
disease processes, abnormal presentations of common

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734
Figure 1. An algorithm approach to bilateral parotid enlargement. BLEC, benign lymphoepithelial cyst; DILS, diffuse infiltrative lymphocyto-
sis syndrome; HIV, human immunodeficiency virus; MALT, mucosa-associated lymphoid tissue.
Figure 2. Percentage of bilateral involvement in parotid enlarge-
ment. BLEC, benign lymphoepithelial cyst; DILS, diffuse infiltrative
lymphocytosis syndrome; HIV, human immunodeficiency virus.
diseases, and rare diseases, which are not well captured by
this algorithm. Regardless, reviewing this algorithm as well
as an updated review of the common disease entities that
underlie bilateral parotid enlargement is of value to the
clinician.
Sialadenosis
Sialadenosis (sialosis) is associated with nutritional and hor-
monal disturbances, particularly chronic malnutrition, obesity,
diabetes mellitus, alcoholism, liver disease, and eating disor-
ders.8 Many drugs have been implicated in sialadenosis, most
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OtolaryngologyHead and Neck Surgery 148(5)
prominently antihypertensives. Some cases of sialadenosis
have no known underlying systemic disease.9
Sialadenosis is common among patients with eating disor-
ders and chronic malnutrition.10 It afflicts 10% to 50% of
patients with bulimia nervosa.11,12 Given that 19% of college-
aged females may have bulimia nervosa, it is a common dif-
ferential diagnosis of bilateral parotid involvement.11
With the rising incidence of metabolic syndromes, dia-
betes mellitus is an increasingly important cause of sialade-
nosis. Scully et al13 reported that 49% of sialadenosis
patients were diabetic, although diabetes and liver disease
often coexist in patients. One study showed that 48 of 200
diabetic patients (24%) had asymptomatic bilateral parotid
enlargement.14 In some cases, parotid enlargement preceded
the diagnosis of diabetes.6 Some authors have proposed that
asymptomatic parotid gland enlargement warrants a search
for diabetes and that salivary composition and function have
potential to contribute to the clinical diagnosis and staging
of diabetes. Although still controversial, abundant research
has focused on the specific changes in secretory protein
expression and salivary flow in salivary glands of diabetic
patients, which may contribute to the oral complications of
diabetes.15
Sialadenosis is also frequently found in patients with alco-
holism and alcoholic cirrhosis, with an estimated incidence
of 30% to 86%.8,16 Whether alcoholism without cirrhosis and
other causes of cirrhosis can result in sialadenosis had been
debated. A recent study found sialadenosis in 28 of 300 liver
transplant candidates (9.3%). Among these 28 patients with
sialadenosis, 39.3% had alcoholic cirrhosis, and 60.7% had
nonalcohol-related liver diseases. The study suggested that
cirrhosis, irrespective of its etiology, may lead to the develop-
ment of sialadenosis.17
The pathogenesis of sialosis is not well established but
may involve a neuropathic process of the autonomic inner-
vations of the salivary glands in the setting of systemic
Chen et al
demyelinating polyneuropathy. Autonomic neuropathies are
noted in patients with alcoholism, nonalcoholic liver dis-
eases, and diabetes. Dysfunction of autonomic regulation
leads to imbalance of acinar protein synthesis and protein
secretion. Mandel and Surattanont1 proposed that the histo-
logic findings of enlarged acini and glandular hypertrophy
are a result of retained zymogen granules in the acinar cells.
Ultrastructural studies of the sialosis tissue also showed evi-
dence of axonal and myoepithelial cell degeneration with
swelling of axon fibers and vacuolization.18
More recently, different authors have described different
histopathology pictures in diabetic and alcoholic sialosis.
Diabetic sialosis has smaller acini, greater fatty infiltration
in the glandular stroma, and normal-appearing epithe-
lium.7,15 On the other hand, alcoholic sialosis exhibits a
reduction in the proportion of fatty tissue of stroma and a
significant growth of ductal epithelium that contributes to
increase the caliber of the striated ducts.7 Also noted in
alcoholic sialosis are accumulation of secretory granules in
the acinar cells cytoplasm and enlarged excretory ducts.15
Infection
The infectious causes of bilateral parotid enlargement
include viral mumps, HIV, acute suppurative parotitis,
tuberculosis, and bilateral parotid abscess. Of these, viral
mumps and HIV are bilateral more than half of the
time,3,19,20 whereas the rest are less likely to be bilateral
(Figure 2).
Acute suppurative parotitis is bacterial infection of the
parotid gland associated with dehydration, immune defi-
ciency, and premature babies.19,21-23 Fattahi et al21 reported
that acute suppurative parotitis afflicts up to 0.02% of all
hospitalized patients and 0.04% of postoperative patients.
Tuberculosis is a rare cause of parotid enlargement. It is
often mistaken for parotid tumors.24,25 In a series of 215
parotid tumor histology examinations, 6 were found to have
tuberculosis instead.26 In 49 cases of tuberculosis parotitis,
only 1 presented with bilateral parotid involvement.27
Viral mumps, acute suppurative parotitis, and abscess
can present acutely with pain. Nodular parotid lesions are
present with HIV and abscess, and sometimes in tuberculo-
sis (Figure 1).
Viral Mumps
Recently, large viral mumps outbreaks have been reported in
developed countries.2-4 The resurgence of this disease comes
with new challenges as its epidemiology has changed.
Adolescents and young adults were affected in these out-
breaks, compared with older reports in which young children
were the most likely victims. Parotid symptoms may be
absent in 10% to 30% of symptomatic cases.2 The report that
some of the mumps patients had received vaccination brings
to light the moderate efficacy of the mumps vaccine.4 New
research is focused on improving the mumps vaccine and
studying the immunological markers of mumps immunity.
When the diagnosis of mumps is considered, the clinician
may obtain the diagnosis through laboratory testing. Often,
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735
a complete blood count will depict a normal white blood
cell count with a possible viral-induced lymphocytosis.
Amylase can elevate during mumps, and it is helpful to
examine subtypes to distinguish mumps parotitis (amylase-
S) and pancreatitis (amylase-P). Serum lipase is elevated in
pancreatitis. Ultimately, definitive diagnosis can be made
through serologic testing based on virus-specific IgM anti-
body as measured by direct or indirect enzyme-linked
immunosorbent assay. A rise in IgG titers seen between the
acute and convalescent phases of disease can be difficult to
interpret due to cross-reactivity of paramyxovirus. Virus iso-
lation from urine, saliva, semen, or cerebrospinal fluid is
limited to the period of viral replication, which occurs 7
days before and until the first week after the onset of clini-
cal symptoms. The window to isolate the virus is often
passed by the time of consideration. Rapid polymerase
chain reaction evaluation of cerebrospinal fluid for viral
mumps RNA may be performed if there is concern for neu-
rologic involvement.28
HIV
Since the introduction of highly active antiretroviral therapy
(HAART) in the mid-1990s, there has been a decline in the
prevalence of oral manifestations of HIV infection.29
However, the incidence of HIV-associated salivary gland
diseases, mostly involving parotid glands, has remained the
same in developing countries30 and even has increased in
developed countries.31 Parotid gland enlargement reportedly
occurs in approximately 1% to 10% of HIV-infected
patients.5 Etiologies of parotid enlargement specific to HIV-
seropositive patients include hyperplastic lymphadenopathy,
benign lymphoepithelial cysts (BLEC), and diffuse infiltra-
tive lymphocytosis syndrome (DILS).
Benign lymphoepithelial cysts occur in 3% to 6% of
HIV-positive adults and in 1% to 10% of HIV-positive chil-
dren.5 HIV-associated BLEC often presents early in the
course of HIV infection with slowly progressive but asymp-
tomatic parotid gland enlargement. In the era before the
widespread use of HAART, the prevalence of DILS was at
3% to 4% of HIV-positive patients.32 Despite the success of
HAART, Ceballos-Salobrena et al33 reported increased inci-
dence of parotid gland enlargement in HIV-positive patients
(4.5%) on HAART. A known adverse effect of protease
inhibitors is fat accumulation in various parts of the body
such as the back of the neck (buffalo hump) and intra-
abdominal region. Protease inhibitors have been suggested
to cause fatty infiltration of the parotid gland or parotid
lipomatosis, resulting in glandular swelling.33
Neoplasm
Warthin tumor, mucosa-associated lymphoid tissue (MALT)
lymphoma, and oncocytomas are the neoplasms that may
present with bilateral parotid enlargement. Warthin tumor
accounts for 6% to 13.5% of all parotid tumors34; only
5.7% to 14% are bilateral.34-36 There is increased risk of
bilateral Warthin tumor in smokers.35
736
Mucosa-associated lymphoid tissue lymphoma involving
the parotid gland is less common but can be seen in patients
with Sjogrens syndrome, HIV, or chronic sialadenitis.37,38
The parotid glands may be the primary site of the MALT
lymphoma.39,40 Berger et al41 reported 3 cases of parotid
involvement in 42 cases of MALT lymphoma, whereas
Takahashi and colleagues42 found 7 cases of parotid enlar-
gement in 10 patients with MALT lymphoma. Bilateral par-
otid enlargement due to MALT lymphoma is very rare,
noted by asymmetric enlargement.40
Oncocytomas account for less than 1% of salivary gland
tumors.1 In a review by Hyde et al,43 only 20 cases of bilat-
eral oncocytoma have been reported in the literature
between 1927 and 2008. Brandwein and Huvos44 reported
that 7% were bilateral among 68 cases.
Of the 3 neoplastic etiologies, only MALT lymphoma is
reportedly rapid onset when causing parotid enlargement.
None of them are likely to cause pain, but they are all nodu-
lar.1 Both Warthin tumor and MALT lymphoma can have a
mix of solid and cystic components.1,40,45
Autoimmune
Multiple autoimmune diseases may involve the salivary
glands. Parotid enlargement is most often seen in Sjogrens
syndrome (SS), present in up to 55% of SS patients26 and
bilateral 75% of the time.46 Parotid enlargement in SS can be
multicystic.47,48 Both SS and recurrent parotitis may present
with parotid enlargement that fluctuates in size. Chronic
sclerosing sialadenitis, also referred to as a Kuttners tumor,
displays an elevated IgG4/IgG ratio, is SS-A and SS-B nega-
tive, and is a steroid-responsive sclerosis of the salivary
glands that is a pertinent negative in the differential diagnosis
of SS. Chronic sclerosing sialedenitis often affects the lacri-
mal and submandibular glands, whereas bilateral parotid dis-
ease has yet to be reported to date.49
Only 4% to 6% of sarcoidosis patients may have parotid
involvement50; however, it is bilateral in 30% to 70% of these
patients.26 Orofacial manifestations such as salivary gland
swelling should prompt workup for systemic sarcoidosis.51
Salivary gland involvement is less common in Wegeners
granulomatosis (WG), reported in 3 of 70 cases of WG.52
Specks et al53 reported that 1 in 5 cases of salivary enlarge-
ment due to WG were bilateral, whereas Jones et al54 found
2 bilateral cases among 32 cases. Of note, salivary gland
enlargement may be the early feature of a limited form of
WG in which only 67% of patients are antineutrophil cyto-
plasmic antibody (ANCA) positive.1 This may alert the clin-
ician to consider an autoimmune workup.
Iatrogenic
Bilateral parotid enlargement can be a rare complication of
medical and surgical therapies.
General Anesthesia
Parotid swelling is a rare complication of general anesthesia,
termed anesthesia mumps. It occurs a few hours after general
anesthesia with endotracheal intubation, bronchoscopy, and
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OtolaryngologyHead and Neck Surgery 148(5)
upper gastrointestinal endoscopy.55 Patients complain of mild
facial pain usually without difficulty swallowing or breathing.
Different combinations of unilateral or bilateral parotid and
submandibular swelling have been described. The pathophy-
siology is not clear but may involve trauma, infection, and
salivary stasis due to dehydration. Postoperative sialadenitis
often spontaneously resolves within 5 to 7 days without
sequelae.56
Iodide Mumps
Iodide mumps is seen after injection of iodinated contrast
media for radiographic studies. This disorder presents as
acute or delayed painless swelling, predominantly in the
submandibular and parotid glands, and almost always bilat-
eral.57 There have been 30 reported cases of iodide mumps
between 1956 and 2010.58 The incidence of iodide mumps
is increasing with the escalating use of computed tomogra-
phy and angiography.59,60 It occurs with both ionic and non-
ionic contrast agents, but 90% occur with ionic agents.61
In patients with immediate swelling of bilateral parotid
glands within 1 hour of contrast administration, a hypersen-
sitivity reaction is the likely mechanism.62 Delayed onset of
parotid swelling 6 to 12 hours after contrast administration
may be attributed to toxic accumulation of iodine in the
salivary glands.63
Radiation Sialadenitis
Radiation sialadenitis is salivary gland toxicity occurring in
up to 18% to 26% of patients receiving radioactive iodine
therapy for thyroid cancer.64,65 Alexander et al66 reported
that among 203 patients with salivary gland toxicity, 40
patients had bilateral parotid swelling. Bilateral parotid
gland and/or submandibular gland enlargement are more
common than unilateral involvement.66
With external beam radiation, symptoms are dependent
on radiation dosage.65 Low-dose radiation (20-30 gy) may
cause reversible damage, whereas high-dose radiation (501
gy) often causes irreversible injury. The changes occur in 3
stages: stage I, mild inflammatory interstitial change with
moderate individual gland acini atrophy; stage II, increased
inflammatory infiltrate with fibrosis of the interstitium with
epithelial metaplasia in the ductal system; and stage III, cir-
rhotic parenchymal alteration with clear inflammatory activ-
ity with near-complete parenchymal atrophy. The time
frame for stage I changes is on the order of days, and stage
III changes are rarely seen before 3 months and may take
years to fully develop. The average time to the development
of late-stage disease is 4.8 months.65,67
Miscellaneous Causes
Kimura Disease
Kimura disease is a rare, chronic inflammatory disease that
presents with painless soft tissue swelling around the head
and neck area.68 Kimura disease is more prevalent in
Eastern Asian populations; however, rare cases have been
reported in patients of European, African, Hispanic, and
Arabic descent. Eighteen patients in 54 cases of Kimura
Chen et al
disease had parotid enlargement.69 A unilateral parotid mass
is more common; however, bilateral parotid involvement
has been reported.69,70
Solitary or multiple lesions are found in deep subcutaneous
tissue, with pruritus in the overlying skin.71 It is frequently
associated with regional lymphadenopathy involving parotid
glands and periauricular, axillary, and inguinal lymph nodes.68
Peripheral blood eosinophilia and elevated serum IgE are
almost always present.68,71
Polycystic Parotid Disease
Polycystic parotid disease presents with intermittent painless
swelling of the parotids. It is seen in female and young adult
patients. There have been 13 reported cases of polycystic par-
otid disease since 1962, 10 of which were bilateral.72
Implications for Practice
History and physical exam findings such as disease onset,
pain, and nodularity are key elements in the algorithm to
quickly narrow the differential diagnosis of bilateral parotid
enlargement. Following the algorithm presented here should
allow the clinician to rapidly narrow the differential diagno-
sis and arrive at a diagnosis rapidly without ordering unne-
cessary tests and wasting resources. New research and case
reports will allow continued update and improvement of the
diagnostic algorithm.
Acknowledgment
The authors acknowledge Andrew Kleinberger, MD for his input
to this manuscript.
Author Contributions
Si Chen, design, acquisition of data and analysis and interpretation
of data, drafting of the article; Benjamin C. Paul, design, acquisi-
tion of data and analysis and interpretation of data, drafting of the
article; David Myssiorek, concept and design, interpretation of data.
Disclosures
Competing interests: None.
Sponsorships: None.
Funding source: None.
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