Inflammatory Disorders of The Salivary Glands

Inflammatory Disorders of 85
the Salivary Glands

Neal M. Jackson | Jenna L. Mitchell | Rohan R. Walvekar
Key Points
■ Sialadenitis, most commonly caused by sialolithiasis, should be treated medically in the acute
care setting with warm compresses, sialogogues, hydration, and antibiotics. Chronic or
persistent disease may require minimally invasive sialendoscopy for diagnostic and therapeutic
purposes.
■ Sialendoscopic techniques include endoscopic visualization of stenosis or calculi, balloon dilatation
of stenoses, fragmentation of large stones with Holmium laser, and ensnarement of stones with a
wire basket.
■ Although imaging (ultrasound, computed tomography, or magnetic resonance imaging) is an
appropriate ancillary test for many cases of sialadenitis, the diagnosis of most viral (mumps, HIV)
and granulomatous (actinomycosis, cat scratch disease, toxoplasmosis) salivary gland infections
requires specific serology antibody testing, skin testing, or fine-needle aspiration.
■ Sjögren’s syndrome, a chronic autoimmune disorder characterized by destruction of the bilateral

salivary and lacrimal glands that leads to dry mouth and dry eyes, is managed with symptomatic
treatment (salivary substitutes, sialogogues, frequent dental examinations, eye drops, and
lubricants). Some patients with recurrent sialadenitis may benefit from dilation of salivary gland
ducts or possibly even gland excision.
I nflammatory disorders of the salivary glands can vary in their The precise etiology of sialolithiasis remains unknown. Sali-
cause, chronicity, treatability, and overall prognosis. The most vary stasis and inflammatory changes to the ductal system are
common cause is obstruction of salivary outflow, most com- important factors that contribute to stone formation. It is
monly from a sialolith in the duct. Salivary gland infections— believed that intermittent salivary stasis results in an alteration
including bacterial, viral, fungal, parasitic, and protozoal of the mucoid elements of saliva, which leads to the formation
infections—are another major cause of sailadenitis. Addition- of an organic gel. This gel becomes the framework for the
ally, systemic medical pathologies, such as autoimmune diseases deposition of salts, which leads to the development of calculi.
like Sjögren disease, can also affect the salivary glands. Serum levels of calcium and phosphorous do not seem to be
related to stone formation.5
The relationship between sialolithiasis and chronic sialade-
SIALOLITHIASIS nitis might differ among salivary glands.6 In the submandibular
Sialolithiasis is the formation of calculi in the ductal system of gland, development of a sialolith might be the primary event
the salivary glands. It is the most common cause of inflamma- that results in stagnation of saliva and inflammation, which
tion in the salivary glands.1 The submandibular gland is most encourages retrograde bacterial migration that can result in
commonly affected, and 80% to 90% of stones develop in the sialadenitis. In contrast, inflammation and ductal injury in the
Wharton duct. Approximately 10% to 20% of calculi form in parotid gland from chronic sialadenitis is believed to be the
the parotid (Stensen) duct, and 1% form in the sublingual inciting process for sialolithiasis. Additionally, several other
duct.2 Patients in their fifth to eighth decades of life represent factors might account for the propensity of salivary stones to
most cases. Sialolithiasis in children is rare; however, if afflicted, form in the submandibular gland. The Wharton duct is longer,
they most commonly come to medical attention at about 10 wider, more tortuous, and angulated against gravity as it courses
years of age.3 Men tend to develop calculi more frequently than around the mylohyoid muscle; all of these contribute to slower
women. salivary flow rates and consequently poor salivary egress into the
Salivary stones are composed predominantly of calcium oral cavity and thus promote stasis. Also, the saliva produced by
phosphate and carbonate in combination with an organic the gland itself is more viscous and has a higher calcium and
matrix of glycoproteins and mucopolysaccharides. Small phosphorous concentration.7 In the parotid gland, stones are
amounts of other salts such as magnesium, potassium, and most commonly located at the hilum or parenchyma. Sialoli-
ammonium are also involved in stone formation.4 thiasis in the submandibular gland tends to develop in the duct.8
1223
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1224 PART VI | HEAD AND NECK SURGERY AND ONCOLOGY
Patients with sialolithiasis are seen with recurrent episodes

of postprandial salivary colic with pain and swelling. The patient
might also have a history of multiple cases of acute suppurative
sialadenitis. On physical examination, bimanual palpation
sometimes reveals the presence of a palpable stone involving
the submandibular duct. Parotid stones might be noted at the
orifice of the Stensen duct or along the course of the duct.
Examination may also reveal asymmetric findings in the patency
of salivary ducts and quality of saliva, and obstructed ducts may
show lack of salivary flow on bimanual palpation or massage of
the gland, or they may demonstrate mucoid, particulate, or
mucopurulent saliva. Consequently, patients will frequently
come in with symptoms of foul-tasting fluid on massaging
the obstructed gland that can point to the etiology of the
symptoms.
Imaging of the salivary glands for sialolithiasis may be
accomplished with ultrasound, computed tomography (CT), or
magnetic resonance imaging (MRI).9 Plain radiographs that
use intraoral or occlusal views were traditionally helpful for
identification of radiopaque stones but are no longer routinely
used, because they miss radiolucent stones and can confuse
sialoliths with other calcifications in the area such as phlebo-
liths, atherosclerosis of the lingual artery, or calcified cervical
lymphadenopathy.
Instead, newer imaging techniques are commonly used.
FIGURE 85-1. Computed tomography with bony windowing that reveals
Ultrasound has proven value in the diagnosis of sialolithiasis multiple hyperdense sialoliths in the right submandibular gland.
and has the ability to detect 90% of stones greater than 2 mm.10
Although the accuracy of ultrasound is dependent on the oper-
ator, in general, it is very useful for several reasons. Ultrasonog- Management of salivary stones depends on the size, loca-
raphy is cost-effective, avoids radiation exposure, is repeatable tion, orientation, shape, number, whether the stone is impacted
and dynamic, provides excellent definition of the salivary gland or mobile, and the surgeon’s experience.15,16 Additionally, the
and mobility of the calculus, and also can be utilized intraop- earlier the stone is removed, the better the prognosis, because
eratively for stone localization.11 CT scanning with fine cuts (1 the longer stones occupy ducts, the larger and more immobile
to 2 mm) is extremely accurate at detecting salivary stones. they may become.17
Contrast is avoided, because opacified blood vessels can be Initial nonsurgical management of patients with sialolithia-
confused with sialoliths. However, the physician must not sis consists of the use of sialagogues, local heat, hydration, and
ignore the possibility of a synchronous neoplastic process. Con- massage of the involved gland. If salivary gland infection is
sequently, in cases where the history, physical examination, or suspected, prompt antimicrobial therapy should be initiated.6
other radiologic findings are suspicious of a neoplastic process Surgical intervention for sialolithiasis depends on the ana-
in addition to an inflammatory condition, a CT scan with tomic location of the stone. Submandibular stones that are
and without contrast should be obtained.12 Findings typically palpable in the mouth and no more than 2 cm from the duct
include an enlarged gland and dilatation of the duct orifice distal to the posterior edge of the mylohyoid muscle can
(Fig. 85-1).
On MRI, the calculus is seen as a low signal intensity focus
on both T1- and T2-weighted images.9 Digital subtraction
sialography, which lessens the interference of surrounding
bony structures, can also be used to investigate sialolithiasis,
because it can detect radiolucent stones with a reported sensi-
tivity of 95% to 100%.13 Several disadvantages are inherent to
sialography. It is an invasive technique with the possible side
effects of contrast material. Sialography is also contraindi-
cated for stones located in the oral portion of the Wharton
duct and in cases of active infection. MR sialography, which
uses saliva as the contrast medium, is a relatively new and non-
invasive technique being used to evaluate the salivary duct
system (Fig. 85-2). Studies indicate that MR sialography of the
submandibular duct with evoked salivation has accuracy
similar to that of digital sialography and is superior to ultra-
sound.10 MR sialography is a better alternative in patients
with contraindications to digital sialography. However, patho-
logic diagnosis in this setting is difficult, and the ductal meta-
plasia of sialolithiasis secondary to stone formation might be
misinterpreted with mucoepidermoid carcinoma.5 Ultrasonog-
raphy and CT scanning are first-line imaging techniques for
evaluation and management of sialolithiasis. MRI sialography,
digital sialography, and three-dimensional reconstructions to
facilitate virtual salivary endoscopy are reserved for complex FIGURE 85-2. Magnetic resonance sialography of right-sided parotid duct
cases.14 shows multiple areas of stenosis and dilation.

85 | INFLAMMATORY DISORDERS OF THE SALIVARY GLANDS 1225
Sialoendoscope
Submandibular duct
Introducer sheath
FIGURE 85-3. Sialoendoscope inserted through introducer sheath in cannulated papilla of submandibular duct.
sometimes be removed by simply milking the stone through the in size and have an interventional irrigation port that permits
duct opening manually or making a transoral incision. Tradi- intervention using a variety of tools to manage salivary stones
tionally, proximal, hilar, or intraglandular stones; impacted and other obstructive pathology, such as stenosis (Fig. 85-3). A
stones; and large stones or megaliths in the submandibular variety of interventional tools have also been developed to
gland would be managed with a submandibular gland resec- provide fast and nontraumatic dilation of the salivary ducts and
tion. The anatomy of the Stensen duct makes the management papillae to facilitate the introduction of the endoscope and
of parotid stones more difficult, because manipulation of the instruments into the cannulated papilla and the ductal
duct may be complicated by a high incidence of stricture and system.18,19 Salivary endoscopy has gained popularity recently as
frequently requires the use of a temporary stent. However, the a diagnostic and therapeutic tool. Stones and strictures can be
traditional management of parotid stones includes transoral directly visualized, and stones can be removed using a wire
approaches, continued medical management, or parotid gland basket to ensnare them; if the stones are too large for the wire
excision. basket, they may be fragmented into smaller pieces using a
Salivary endoscopy has caused a paradigm shift in the man- holmium laser or lithotripsy (Fig. 85-4).
agement of salivary stones. Today, using a combination of endo- If this proves ineffective, or the stone is impacted, the com-
scopic techniques combined with transoral or external bined approach with an external incision can be used. The
approaches, also known as combined or hybrid techniques, it is combined approach involves visualization and localization of
possible to provide a safe, effective, gland-preserving alternative the stone by endoscopy or ultrasound and removal of the stone
with success rates between 80% and 100%. Sialendoscopy uses by making an incision into the duct. When exploring the duct,
miniature, semirigid endoscopes that range from 0.8 to 1.6 mm submandibular stones can be excised via an intraoral approach;
FIGURE 85-4. Sialendoscopic visualization of a stone in the salivary duct (left) before grasping and removal of the stone with a wire basket (right).

FIGURE 85-5. Endoscopic view of stenotic salivary duct before (left) and after (right) balloon dilatation.
however, parotid stones may require a partial or complete out the intraductal system and dilate the ducts.24 Sialendoscopy
parotidectomy incision and elevation of the superficial muscu- serves as a diagnostic and interventional tool. Generally, if the
loaponeurotic system flap to gain access to the stone. At the patient suffers from more than one acute attack per year, inter-
conclusion of the procedure, a salivary stent may be left in place ventional sialendoscopy may be considered.26
for 2 to 4 weeks to prevent stenosis or stricture of the duct or Diagnostic endoscopy can improve symptoms by washing
papilla.20 out the salivary ducts with a continuous normal saline lavage,
intraglandular steroid instillation, and hydrostatic dilation of
the ductal system. Salivary stenoses diagnosed on endoscopy
CHRONIC SIALADENITIS require further management depending on the severity, loca-
Chronic sialadenitis is a localized condition of the salivary tion, and length of the stenosis. Salivary stenosis can be dilated
gland characterized by relapsing and remitting episodes of pain endoscopically using balloon dilators or combined approach
and inflammation. The submandibular gland is the most fre- techniques (Figs. 85-5 and 85-6).
quently affected site.21 The initial inciting factor is believed to Additionally, stents may be used to prevent stricture refor-
be salivary duct obstruction, which results in salivary stasis and mation and can be kept in place for up to 4 weeks (Fig. 85-7).
eventually in ascending bacterial infection. The most common If the above methods prove ineffective, a final strategy is surgi-
cause of ductal obstruction is sialolithiasis. Additional causes cal removal of the gland.26 Invasive techniques to induce gland
include stricture of the salivary duct, extrinsic compression by atrophy, such as tympanic neurectomy and parotid duct liga-
tumor, stenosis secondary to scar in adjacent tissue, congenital tion, are rarely if ever performed.
dilation, and foreign body.22 Salivary stasis from obstruction Patients with chronic sialadenitis typically show punctate
predisposes patients to episodes of infection and inflammation. sialectasis and dilatation of the peripheral ducts upon imaging.
Recurrent inflammatory reactions result in multifocal wall Imaging modalities include ultrasound, CT, conventional MRI,
irregularities, which consequently form strictures.23 Chronic and MRI sialography. Ultrasonography can be used to visualize
inflammation can also cause progressive acinar destruction both dilatated ducts and calculi while the patient is in the clinic;
with fibrous replacement, thereby resulting in glandular it has also been used intraoperatively to aid in visualization of
atrophy and sialectasis.24 the ductal system.
Clinically, patients experience recurring episodes of sudden-
onset swelling and tenderness of the affected gland. A low-
grade fever can occur in association with episodes, and no
known relationship with meals or seasons has been found.25
Patients frequently report an initial episode of acute suppura-
tive (bacterial) sialadenitis; asymptomatic intervals might range
from a few weeks to months. Physical examination reveals
enlargement of the gland, and frequently mucopus may be
seen draining from the ductal orifice. Mucopus is more viscous
than saliva, and it results in obstruction of the ductal lumen
and salivary stasis. Occasionally, pus can be viewed in patients
with chronic sialadenitis, but this is probably an acute bacterial
sialadenitis superimposed upon the chronic condition. Staphy- Submaxillary
lococcus aureus is the most common causative microorganism gland
involved in adults.24 Wharton
Initial treatment is conservative and involves oral antibiotics, duct
massage, heat, sialogogues, and corticosteroids. Antibiotics are
only effective if acute sialadenitis is present. Corticosteroid Calculus
taper can be used in the short term to decrease inflammation,
and hydration via sialogogues and warm compresses serve to
flush out the precipitated serum proteins within the salivary FIGURE 85-6. Open technique for localization and retrieval of a subman-
ducts. If this treatment fails, sialendoscopy can be used to wash dibular duct sialolith.

A B
FIGURE 85-7. A 1-mm Walvekar salivary stent. Left inferior inset shows double-headed stent with each end ergonomically oriented to the submandibular
and parotid ducts. A, Insertion into right parotid duct. B, Stent inserted and sutured with individual 4-0 nylon stitches or a loop stitch. (Courtesy Hood Labo-
ratories, Pembroke, MA.)
Possible complications of chronic sialadenitis include the of the infection. These might range from acute localized infec-
development of a benign lymphoepithelial lesion, Kuttner tions, such as bacterial sialadenitis, to systemic diseases caused
tumor, and ductal carcinoma.13,27,28 A benign lymphoepithelial by viruses such as the paramyxovirus or the human immunode-
lesion is characterized by a lymphoreticular infiltrate with ficiency virus (HIV). Granulomatous infections might manifest
acinar atrophy, irregularly placed nuclei, and ductal metaplasia; as solitary masses similar to a neoplasm. In chronic infections,
the metaplasia results in the development of epimyoepithelial ductal obstruction might be a predisposing factor.
islands. Women in the fifth to sixth decades of life are more
commonly affected, and a benign lymphoepithelial lesion has ACUTE SUPPURATIVE (BACTERIAL)
been associated with Sjögren syndrome and has also been
termed Mikulicz disease. A benign lymphoepithelial lesion typi-
SIALADENITIS
cally presents as an asymptomatic mass. Fine-needle aspiration Acute sialadenitis is typically a bacterial inflammation of the
(FNA) may be used for diagnosis and allows for a nonsurgical salivary glands, which appears as rapid, diffuse swelling and
approach to management.29 However, patients must be fol- pain over the affected gland in addition to systemic manifesta-
lowed because of reports of malignant transformation.28 tions such as fever, chills, and malaise. Acute infection of the
Kuttner tumor, or chronic sclerosing sialadenitis, is a benign salivary glands is caused by retrograde bacterial contamination
chronic inflammatory process similar to a benign lymphoepi- of the salivary ducts from the oral cavity. Stasis of salivary flow
thelial lesion. However, the lesion occurs almost exclusively in secondary to dehydration or significant hemorrhage permits
the submandibular gland and is characterized by a progressive retrograde migration of bacteria and produces suppurative
fibrosis and parenchymal atrophy. Kuttner tumors are most infection of the gland parenchyma. The parotid gland is most
common in the fifth through seventh decades of life, and susceptible to such infections, a fact attributed to the difference
women have a slightly higher incidence of occurrence.30 The in saliva composition among the various glands. The parotid
clinical presentation involves firm, painful swelling of the gland gland produces saliva that is mainly serous, whereas saliva from
that is usually unilateral. Periductal fibrosis and ductal ectasia the submandibular and sublingual glands is primarily mucoid.
occurs in early stages of the disease, caused by foci of chronic Serous saliva, unlike mucinous saliva, lacks lysosomes, immuno-
inflammation. However, as the disease progresses, fibrosis, globulin A antibodies, and sialic acid, all of which have antimi-
acinar atrophy, and ductal dilation increase. Consequentially, crobial properties. In addition, the saliva from the submandibular
the entire gland becomes fibrotic, and inflammation decreases.31 and sublingual glands contains high-molecular-weight glyco-
Histologically, a heavy lymphoid infiltrate is found among dis- proteins that competitively inhibit bacterial attachment to the
crete tubular structures with regularly aligned nuclei, which epithelial cells of the salivary ducts.32 Several predisposing
differentiates them from a benign lymphoepithelial lesion. factors might lead to acute sialadenitis. These include diseases
Again, careful and routine assessment of patients with chronic such as diabetes mellitus, hypothyroidism, renal failure, and
sialadenitis is underscored by reports of the development of Sjögren syndrome. In addition, medications can reduce salivary
malignancies that include salivary ductal carcinoma.32 Symp- flow through multiple mechanisms (Fig. 85-8).
tomatic management of Kuttner tumor can be accomplished by Mechanical impairment of salivary flow also predisposes to
sialendoscopy to remove sialoliths using a wire basket to retrieve acute infection. Stenosis of the salivary ducts secondary to
stones. Unfortunately, many of these patients need definitive trauma or a foreign body has been reported to result in acute
treatment with gland excision, especially in later stages of the sialadenitis. Sialolithiasis, more frequent in the ducts of the
disease. Sarcoidosis, lymphoepithelial sialadenitis, and follicu- submandibular and sublingual glands, might also contribute to
lar lymphoma are included in the differential diagnosis.33 acute infection but more commonly produces chronic salivary
gland infection.29 Acute bacterial submandibular sialadenitis is
a community-acquired disease that most commonly occurs
INFECTIONS OF THE SALIVARY from a sialolith in the Wharton duct (see the section on sialo-
liths for more information).24
GLANDS Sialadenitis has also commonly been associated with medi-
Salivary gland infections have a wide range of presentations, cally debilitated and postoperative patients. The incidence of
depending on the etiologic agents involved and the chronicity acute sialadenitis is approximately 0.173 cases per 10,000

The cycle of recurrent sialadenitis bacteria, as well as S. aureus, so methicillin resistance should be
investigated.33,35,36
Drug side effects
Cachexia
On physical examination, the patient might demonstrate
Dehydration signs of systemic dehydration with dry mucous membranes.
Radiation Local findings include tenderness to palpation with warmth
Chemotherapy and induration of the overlying skin. Bimanual palpation of the
Benign lymphoepithelial lesion gland results in suppurative discharge from the red and dis-
Sjögren syndrome tended duct orifice in approximately three fourths of cases.
Stress Multiple glands might be affected, with a reported incidence
of bilateral involvement in up to 25% of cases.37
The laboratory evaluation typically reveals a leukocytosis
Reduced salivary with neutrophilia. Also, signs consistent with dehydration may
secretion occur, such as hypernatremia and elevated blood urea nitro-
gen.38 Imaging of the affected gland with CT or ultrasound for
Ascending abscess formation is indicated in patients who do not respond
oropharyngeal to medical therapy within 48 to 72 hours. Sialography per-
bacterial formed in the acute phases of sialadenitis provides little useful
Duct obstruction contamination information and is contraindicated, because it can exacerbate
Sialolithiasis
Sialectasia the existing inflammation. However, ultrasonography, CT, and
MRI may be used if neoplasms, sialolithiasis, or abscesses are
suspected.38
If there is active drainage from the duct, it can be cultured
Acute to further direct antimicrobial therapy; however, a risk of con-
Sialolithiasis Chronic suppurative
recurrent tamination from the oropharynx exists when culturing puru-
sialadenitis
sialadenitis lent discharge from the Stensen duct. Moreover, caution should
be used during FNA of the parotid gland, because a granu
lomatous infection can result in fistula formation. Cultures
Resolution should be tested for aerobic and anaerobic bacteria, fungi, and
mycobacteria.34,39,40
FIGURE 85-8. Pathophysiology and predisposing factors for the develop-
Although the diagnosis of acute parotitis is usually apparent,
ment of acute and chronic suppurative sialadenitis.
the differential diagnosis for nonparotid swelling that mimics
parotitis includes lymphoma, lymphangitis, external otitis,
operations (0.00173%).34 Patients undergoing major abdomi- Bezold abscess, cervical adenitis, dental abscesses that appear
nal and hip repair surgery have been identified as being at as buccal or masseteric space abscesses, and infected branchial
increased risk for acute suppurative sialadenitis, which is attrib- cleft or sebaceous cysts.37
uted to postoperative dehydration. The disease is most com- Initial treatment of acute suppurative sialadenitis begins
monly reported to occur within the first two postoperative with aggressive medical management. This includes prompt
weeks.34 fluid and electrolyte replacement, antibiotic therapy, oral
The elderly are at a higher risk of developing sialadenitis, hygiene, and reversal of salivary stasis. Stimulation of salivary
often because of a medication-induced decrease in salivary flow. flow is accomplished by the use of sialogogues such as lemon
Drugs that contribute to salivary stasis include anticholinergics drops and orange juice. In addition, capable patients should
and antihistamines. Other predisposing factors to sialadenitis be instructed on regular external and bimanual massage, start-
include dehydration, poor oral hygiene, immunosuppression, ing from the distal bed of the gland and progressing toward
salivary duct obstruction, autoimmune diseases (Sjögren syn- the papillae. Analgesics and local heat application ease the
drome), diabetes mellitus, hypothyroidism, and renal failure. discomfort.
Of the medically ill patients affected by sialadenitis, approxi- Antimicrobial therapy is an essential part of the manage-
mately 25% have a malignant lesion, and another 50% have a ment of acute salivary gland infections. Antimicrobial therapy
preexisting infection elsewhere than the head and neck. Most is initiated empirically toward gram-positive and anaerobic bac-
affected patients are between 50 and 60 years of age; men have teria. However, the recovery of β-lactamase–producing bacteria
a higher incidence, and the right side is involved more fre- in 75% of patients requires the use of augmented penicillin
quently than the left.34 and antistaphylococcal penicillin or a first-generation cephalo-
The past few decades have brought change to the bacterial sporin.3,40 Culture results should be used to further direct anti-
flora of the oral cavity, which affects the management of acute microbial treatment. Methicillin-resistant S. aureus infection
bacterial parotitis. This has occurred for several reasons, among may require the use of vancomycin or linezolid. The use of
which is the increase in nosocomial and opportunistic infec- clindamycin or the addition of metronidazole to the first-line
tions among immunocompromised and ill patients admitted to agents to broaden anaerobic coverage has been advocated by
the hospital. Additionally, improved technology has allowed for some authors.41 Response to antimicrobial therapy is seen
the culture and accurate identification of more microorgan- within 48 to 72 hours of initiating treatment and should con-
isms, especially anaerobes. Finally, the abundant use of oral tinue for 1 week after resolution of symptoms.42
antibiotics in the community has resulted in microorganisms Rarely, conservative measures fail to eradicate the infection,
that can survive in the oral cavity that normally would not. In and surgical drainage of a loculated abscess is necessary. The
addition, antibiotic resistance occurs in organisms that nor- surgical approach involves elevation of an anterior-based facial
mally occupy the oral cavity.24 The most common pathogens flap with abscess drainage by way of radial incisions in the
associated with acute bacterial parotitis are S. aureus and anaero- parotid fascia parallel to the facial nerve branches. A drain
bic bacteria such as Fusobacterium and Peptostreptococcus (gram- should be placed, and wound edges should be loosely approxi-
negative bacilli). Additionally, streptococcal species and aerobic mated; the central aspect is left to heal by secondary intention.
gram-negative bacilli have been reported. Nosocomial parotitis Sialendoscopy is generally contraindicated in acute sialade-
is associated with aerobic and facultative gram-negative nitis, because inflammation of the ducts makes dilation difficult

and increases the risk of iatrogenic ductal trauma from rigid unilateral; if involvement is bilateral, the symptoms are more
and semirigid instrumentation. Exacerbation of the infection prominent on one side. Afflicted patients tend to experience
is also a potential risk. exacerbations every 3 to 4 months, and each might last days to
Complications of acute suppurative parotitis are unusual. weeks.38 The first signs manifest during the first 1 to 2 years of
Suppuration usually confined to the duct lumen might eventu- life, but the disease is usually not diagnosed until after three to
ally erode through the epithelium into the interstices of the four episodes by the age of 3 to 6 years. Boys are more fre-
parenchyma, creating multiple small abscesses that might quently affected than girls. Although it almost always univer-
coalesce into larger collections that can infiltrate a number of sally resolves during puberty, RPC can lead to severe destruction
potential spaces of the neck. Osteomyelitis, thrombophlebitis of the glandular parenchyma with a functional loss of 50% to
of the jugular vein, septicemia, respiratory obstruction, and 80%. Thus the need to detect and treat early is paramount.
death are potential sequelae of suppurative parotitis. Rupture Risk factors include congenital abnormalities or strictures of
through the floor of the external auditory canal; spontaneous the Stensen duct and a history of viral mumps, trauma, or
drainage through the cheek; and extension to the face, neck, foreign bodies within the duct.34 Evidence also suggests that
and mediastinum have also been reported.43,36 Facial nerve upper airway infections result in dehydration, which can fuel
paralysis, whether complete or incomplete, is uncommon. The subsequent flare-ups.49
etiology of paralysis is unknown but is thought to be due to The cause of RPC remains unknown, although multiple
perineuritis, the virulence of the offending organisms, or acute etiologies have been proposed. Several authors advocate that
nerve compression. Facial nerve paralysis with a palpable mass congenital ectasia of portions of the secondary ductal system
is highly suggestive of an underlying malignancy, and this must predisposes children for bacterial colonization that leads to
be ruled out until resolution of the inflammatory process with recurrent parotitis.50 Staphylococcus aureus and Streptococcus viri-
full recovery of nerve function.43,44 dans are the most commonly isolated organisms from the
parotid ducts of patients. A familial form of RPC has been
described with autosomal inheritance.51 Immunologic abnor-
NEONATAL SUPPURATIVE PAROTITIS malities with isolated deficiencies in immunoglobulins G3 and
Infections of the salivary glands are uncommon in the neonate. A have been associated with recurrent parotitis. In addition,
When infections do occur, they are termed neonatal suppurative parotid swelling might be the sole manifestation of juvenile-
parotitis (NSP), and the parotid gland is most often involved. onset primary Sjögren syndrome. Several viruses might also
Salivary gland infection is more common in preterm and play a role in RPC. A history of mumps parotitis often exists,
male neonates, as are dehydration and nasogastric feeding.6,15 and repeated multiplication of the Epstein-Barr virus (EBV) in
S. aureus is the most common pathogen, but group B and viri- the parotid gland might be responsible for establishing recur-
dans streptococci, Streptococcus pyogenes, Peptostreptococcus and rent parotid gland inflammation; RPC has a reported incidence
Staphylococcus species (coagulase negative), Bacteroides melanino- of 20% in HIV-infected children.52,53
genicus, and Fusobacterium nucleatum have also been implicated The histologic appearance of affected parotid glands
in NSP.45,46 The oral cavity is replete with anaerobic bacteria and demonstrates massive periductal lymphocytic infiltration. The
serves as the portal of entry in most patients through retrograde intraglandular ducts are dilated and measure approximately 1
transmission of bacteria.40 This is especially common in the to 2 mm in diameter.54
event of salivary stasis or dehydration. However, blood-borne Several imaging modalities may be used to study the ductal
bacteria, most commonly gram-negative bacteria, might infect system of patients with RPC. The characteristic finding is sialec-
the salivary glands.47 tasis that on conventional sialography appears as numerous
In addition to fever, anorexia, irritability, and lack of weight scattered, punctate pools of contrast. Ultrasonography of the
gain, other clinical signs of NSP can include swelling and ery- parotid gland reveals an enlarged gland with multiple small
thema of the skin overlying the involved gland. Swelling is hypoechoic areas. These areas represent both sialectasis of the
usually unilateral initially but often becomes bilateral. The gland ducts and surrounding lymphocytic infiltration. Recently, MR
might be tender, and the swelling can be firm or fluctuant. sialography has been reported to be useful in the evaluation of
Diagnosis of NSP is made on the basis of clinical findings RPC.54 It is a noninvasive study that does not require contrast,
and Gram stain and culture of pus from the duct or from FNA and it may be used during acute episodes.
of the gland. Laboratory findings include a leukocytosis with Treatment options range from observation with medical
neutrophilia. Serum amylase levels are usually normal, possibly management to surgery. Initial treatment consists of adequate
because of immature salivary isoenzyme activity.48 Ultrasonog- hydration, pain control, gland massage, local heat, sialogogues,
raphy shows an enlarged gland with hypoechoic areas.46 Initial and appropriate intravenous antibiotics. Empiric therapy
therapy consists of hydration and parenteral antibiotics directed before culture results should consist of a penicillinase-resistant
at S. aureus and gram-negative bacilli, until culture and sensitiv- antistaphylococcal antibiotic. Most patients experience rapid
ity results are available. The presence of methicillin-resistant resolution of swelling and discomfort. For patients with persis-
staphylococci cannot be ruled out. Drainage procedures should tent symptomology, interventional sialendoscopy may serve
be used only when prompt clinical improvement does not both diagnostic and therapeutic goals. The endoscopic view of
occur, when fluctuance of the gland increases, or with an intra- a narrow duct with blanched ductal walls and loss of normal
parotid abscess.41,46 vascular markings is a characteristic finding (Fig. 85-9).
Endoscopic findings include mucus plugs and strictures.
These can be treated with high-pressure balloon dilation and
RECURRENT PAROTITIS OF CHILDHOOD endoscopic removal of debris or saline lavage. Endoscopic irri-
Recurrent parotitis of childhood (RPC) is a rare, nonspecific gation with cortisone and sodium chloride to decrease inflam-
sialadenitis of the parotid gland characterized by periodic epi- mation may also be beneficial.12,55 One treatment is to irrigate
sodes of swelling and pain that typically resolves spontaneously the glands with triamcinolone acetate (Kenalog); 40 units are
prior to the onset of puberty. It is the second most common diluted in 3 to 5 mL of normal saline after completion of
inflammatory salivary gland disease of childhood after mumps. endoscopy for patients with RPC. Sialography, which utilizes
Clinically, patients are seen with recurrent episodes of acute or highly concentrated iodinated oil placed into the duct, may
subacute parotid gland swelling along with fever, malaise, and also serve both diagnostic and therapeutic roles, because it uses
pain, frequently after a meal. Episodes of RPC are commonly an antiseptic solution for visualization of punctate sialectasis

FIGURE 85-9. Endoscopic view of a normal salivary duct (left) and a blanched, narrowed duct with loss of normal vascular markings (right).
and dilatation of peripheral ducts; the solution may linger in retrograde ductal migration does occur. Viral infection of the
the duct for days or weeks and provides prolonged antiseptic salivary parenchyma is not always locally symptomatic, because
effects. Instillation of sclerosing antimicrobials (tetracycline) transmission from blood to saliva occurs without localizing
can also be effective.56 Fortunately, virtually all cases resolve signs in many systemic viral infections, including rabies, hepa-
spontaneously with the onset of puberty or in late adolescence, titis, influenza, and poliomyelitis.
and additional surgical treatment is rarely required.
HUMAN IMMUNODEFICIENCY VIRUS
RADIOIODINE-INDUCED SIALADENITIS HIV is associated with several pathologic processes that involve
Radioiodine has many uses in a variety of thyroid conditions, the salivary glands. These include neoplasms such as Kaposi
namely for treatment of thyrotoxicosis, for ablation of residual sarcoma, benign lymphoepithelial lesions, reactive lymphade-
thyroid tissue after thyroidectomy, and in thyroid cancer surveil- nopathy, sialadenitis and mycobacterial infections, and changes
lance.46 Some studies report that radiation-induced sialadenitis related to antiretroviral therapy.50 HIV-associated salivary gland
occurs up to 18% to 26% of patients with thyroid carcinoma disease (HIV-SGD) is a term used to describe this diffuse enlarge-
who receive radioactive iodine therapy.57,58 Others report subjec- ment of the salivary glands, and it can affect patients through-
tive symptoms of sialadenitis, dry mouth, and dysgeusia in up to out all stages of the disease and may be the initial manifestation
60% of patients and abnormal scintigraphy in up to 69% of of HIV infection.61 Salivary gland involvement usually develops
patients undergoing radioiodine therapy.49,59 Radioiodine- before progression to acquired immunodeficiency syndrome
induced sialadenitis is characterized by an acute, diffuse parotid (AIDS) and may be related to increased viral load.
enlargement, which can be painful or painless. Bilateral involve- The parotid gland is the most commonly affected salivary
ment is reported most often.60 Toxicity to the salivary glands is gland, and it is involved in 1% to 10% of HIV-infected
dose dependent, and although toxicity related to lower doses patients.54,65,66 Parotid swelling is usually due to the develop-
(20 to 30 Gy) is reversible, higher doses (>50 Gy) carry the ment of benign lymphoepithelial cysts (BLECs) within the
potential for irreversible damage.61 Symptoms can be debilitat- gland (Fig. 85-10). These AIDS-related cysts are also referred
ing and may significantly affect quality of life; these include to as benign lymphoepithelial lesions, AIDS-related lymphadenopathy,
chronic pain, constant or recurrent swelling of one or more or diffuse infiltrative lymphocytosis syndrome (DILS). They are so
glands, and dry mouth that causes odynophagia and dysphagia. rare in the HIV-negative population that their presence war-
Because the parotid glands are more predisposed to developing rants HIV evaluation. Salivary secretions have been shown to
severe sialadenitis, gland excision is a less desirable alternative contain low concentrations of the virus and may account for
because of the risk of facial nerve injury associated with gland pathology associated with the HIV-positive patient.67 No other
extirpation for inflammatory salivary gland disease. viruses, such as cytomegalovirus or EBV, have been isolated in
Sialendoscopy is a relatively novel approach in the treatment association with HIV-SGD.
of radioiodine-induced sialadenitis, and success rates vary. An The histologic findings of the salivary glands affected by
interventional sialendoscopy procedure similar to that per- HIV-SGD are varied. The enlarged intraparotid and periparotid
formed for RPC involves gland washouts, removal of debris and lymph nodes demonstrate a uniform follicular hyperplasia
mucus plugs, and dilation of the papilla, ducts, or strictures characteristic of the generalized lymphadenopathy associated
with or without stent placement; this treatment seems to with HIV infection elsewhere in the body. In addition, parotid
provide symptomatic benefit and reduced frequency and inten- nodes contain salivary epithelial structures and epithelial-lined
sity of symptoms. Published studies report success rates that cysts in addition to the follicular hyperplasia. In some cases,
range from 50% to 100% in terms of relieving patients’ symp- diffuse infiltration of the gland by lymphoid elements is appar-
toms with interventional salivary endoscopy.62-64 ent with cystic dilation of the salivary ducts. It is believed that
the surrounding lymphoid hyperplasia results in incomplete
ductal obstruction, which leads to the growth of epithelial
VIRAL INFECTIONS OF cysts.68
Patients with HIV-SGD report a history of progressive, non-
THE SALIVARY GLANDS tender enlargement of one or more of the salivary glands.
Viral involvement of the salivary glands most commonly occurs Findings are bilateral in 80% of patients, and multiple salivary
through hematogenous dissemination, although infection by gland swellings are apparent in 90%. The glandular swellings

shown to induce parotid swelling; this is due to protease inhibi-

tors that cause lipodystrophy in various parts of the body, which
results in fatty infiltration of the parotid gland.72,75
Radiation therapy can be an effective treatment for BLEC,
although its side effects of xerostomia and mucositis can be
permanently troublesome to patients. Some radiation oncolo-
gists may prefer to reserve radiation therapy to treat lympho-
matous lesions or Kaposi sarcoma.
Some controversy exists regarding HIV-SGD and the need
for surgical excision and pathologic examination of an enlarged
salivary gland. In general, in patients with documented HIV-
SGD, it has been demonstrated that the findings of needle
aspiration and CT or MRI are sufficiently typical to provide a
presumptive diagnosis, thereby justifying conservative clinical
observation.76 Surgical excision of BLECs is considered a last
resort, because these lesions are typically multiple, bilateral,
and recurrent. However, the presence of HIV in an individual
should not rule out other salivary gland diseases that affect the
HIV-negative population.77
MUMPS
The term mumps classically defines an acute bilateral, nonsup-
purative, viral parotitis caused by the paramyxovirus. Patients
often experience dysarthria because of inflammation and
trismus.38 Mumps is the most common cause of nonsuppurative
acute sialadenitis, and 85% of cases occur in children younger
than the age of 15 years.51 The disease is highly contagious and
occurs worldwide, with a peak incidence in the spring in tem-
FIGURE 85-10. Intraoperative appearance of a parotid gland cyst in a perate climates and with little variation in the tropics.58
human immunodeficiency virus–seropositive patient. (From Debo RF, The paramyxovirus is an RNA virus that is endemic in the
Davidson M, Petrow CA: Pathologic quiz case 2. Benign lymphoepithelial cyst of community and is disseminated by means of airborne droplets
the parotid gland associated with HIV infection. Arch Otolaryngol Head Neck Surg from salivary, nasal, and urinary secretions. Interestingly, no
1990;116:487.) known animal reservoir, insect vector, or human carrier has
been identified. The disease is maintained by spread from acute
patients.43 Viruses other than paramyxovirus have been impli-
might fluctuate but are generally stable and long standing. cated as causes of acute viral parotitis: these include coxsack
Decreased salivary gland function results in xerostomia and ieviruses A and B, enteric cytopathic human orphan virus,
sicca symptoms. This sicca symptom complex clinically mimics cytomegalovirus, and lymphocytic choriomeningitis virus.64
Sjögren syndrome and has resulted in the classification of DILS. The virus enters through the upper respiratory tract and has
Cervical lymphadenopathy is usually also present.37 an incubation period of 2 to 3 weeks. During this incubation
DILS is characterized by the presence of persistent circulat- period, the virus multiplies in the upper respiratory tract epi-
ing CD8 lymphocytosis and visceral CD8 lymphocytic infiltra- thelium and parotid gland and then localizes to biologically
tion that occurs predominantly in the salivary glands and lungs. active glandular and central nervous system tissue. Patients will
DILS might appear to be similar to Sjögren syndrome but can typically experience a viral prodrome that consists of low-grade
be differentiated by the presence of extraglandular involve- fever, headache, myalgia, anorexia, arthralgia, and malaise just
ment that includes the lung, gastrointestinal tract, and kidneys. before parotid gland symptoms. The parotitis is characterized
The lesion is more focal in DILS, and autoantibodies present by localized pain and edema of the gland along with otalgia,
in patients with Sjögren syndrome will be absent in DILS.63 trismus, and dysphagia. Eating or chewing exacerbates the
FNA is useful in diagnosing salivary gland masses.69 On ultra- pain. In 75% of cases, swelling of the parotid is bilateral and
sound, CT, and MRI, the parotid gland generally demonstrates causes displacement of the pinna.43 Commonly, the gland on
multiple cysts that appear as low-attenuation, thin-walled masses one side will swell first, followed by enlargement of the other
and diffuse cervical lymphadenopathy. Ultrasonography is pref- gland in 1 to 5 days; in rare cases, the submandibular gland
erable in pediatric patients because of the lack of radiation might be affected. Physical examination of the involved gland
exposure and the fact that no sedation is required.70 The MRI will demonstrate nonpitting edema that is tense and firm. The
will show homogenous masses of intermediate signal intensity overlying skin will be stretched with a glazed appearance, but
on proton density and T2-weighted images.71 no erythema or warmth should be present.
Medical treatment of HIV-SGD includes options of close The diagnosis of viral parotitis is confirmed through viral
observation, repeat aspiration, antiretroviral medication, scle- serology. Complement-fixing soluble (S) antibodies against the
rosing therapy, radiation therapy, and surgery.72 Patients with nucleoprotein core of the virus are the earliest antibodies to
DILS and progressive visceral lymphocytic infiltration may be appear. Their levels peak at 10 days to 2 weeks and disappear
treated with corticosteroids and immunosuppressive therapy.73 within 8 to 9 months; therefore these S antibodies are associ-
Because DILS is usually slow growing, any quick increase in ated with active infection. Complement-fixing viral (V) antibod-
gland size should warrant an FNA to rule out malignancy, ies against outer-surface hemagglutinin appear later than S
because HIV patients have an increased risk of transformation antibodies but persist at low levels for years. If serology for
to EBV-associated malignant B-cell lymphoma.74 Antiretroviral paramyxovirus is negative, antibody titers for other viral agents
medications, such as zidovudine, have had varying results in that might also result in parotitis may be obtained. A fourfold
reducing DILS. Highly active antiretroviral therapy has been increase in antibody titer is diagnostic for acute infection.39 The

mumps skin test has no diagnostic value in the setting of acute Clinically, tuberculous salivary gland infection presents in
infection, because dermal hypersensitivity does not develop two different forms. The first is an acute inflammatory lesion
until 3 to 4 weeks after exposure to the virus. A leukocyte count with diffuse glandular edema that may be confused with an
will occasionally be remarkable for leukopenia, and an eleva- acute sialadenitis or abscess. A second chronic, tumorous lesion
tion in the serum salivary-type amylase is also evident. is seen as a discrete slow-growing mass that mimics a neo-
Management of acute viral parotitis involves supportive mea- plasm.13 Constitutional signs that include fever, night sweats,
sures that include bed rest, oral hygiene, hydration, and dietary and weight loss might be absent, and involvement of the facial
modifications to minimize glandular secretory activity. Fever nerve is rare. The chest radiograph is commonly negative but
will usually subside before the resolution of glandular edema, might show evidence of healed granulomatous disease. The CT
which requires several weeks. Complications of mumps virus images of TB infection in the head and neck are described as
include orchitis, aseptic meningitis, pancreatitis, nephritis, and having three patterns. The first occurs early in the course of
sensorineural hearing loss.43 disease and demonstrates involved lymph nodes with nonspe-
The prevention of mumps is by means of vaccination with cific homogenous enhancement. In the second pattern, a nodal
the live attenuated Jerry Lynn vaccine. The vaccine is adminis- mass is apparent with central lucency and thick rims of enhance-
tered subcutaneously, usually in combination with measles and ment and minimally effaced fascial planes. The third pattern
rubella vaccines after 12 months of age. The antibodies pro- appears as fibrocalcified nodes, usually seen in patients previ-
duced persist for at least 5 years. In a recent outbreak on a ously treated for TB.80
college campus, 76% of individuals who came to medical atten- In the setting of a TB infection, the purified protein deriva-
tion with mumps symptoms had previously received the recom- tive skin test should be positive, but it is not a conclusive sign
mended two doses of the measles/mumps/rubella vaccine; because of the high incidence of false positives. FNA biopsy
therefore, prior vaccination should not rule out the possibility may be used for diagnosis with a lower risk of producing a
of mumps.75 The vaccine is contraindicated for immunocom- draining fistula than incisional biopsy. The FNA sample is
promised patients, for those with allergies to neomycin, and analyzed for characteristic cytologic features: granulomatous
during pregnancy.4 inflammation with caseous necrosis and epithelioid histiocytes.
Polymerase chain reaction (PCR) testing can help identify
mycobacteria; however, low bacterial numbers in extrapulmo-
GRANULOMATOUS INFECTIONS OF nary TB lowers the PCR sensitivity.81 In addition, material may
be sent for culture and acid-fast smears; however, cultures may
THE SALIVARY GLANDS take up to 6 weeks to show results.82 Once diagnosed, M. tuber-
Salivary gland involvement frequently arises as a manifestation culosis infection may be treated with triple-drug therapy for a
of a chronic granulomatous disease that involves the lymphatic minimum of 4 to 6 months. When the diagnosis is uncertain
network in and surrounding the parotid gland. Direct infiltra- or the lesion is resistant to medical therapy, complete surgical
tion of the adjacent glandular parenchyma occurs in fulmi- excision is both diagnostic and curative.13
nant cases. Manifestations frequently feature asymptomatic
gradual enlargement of a nodule within the gland substance, NONTUBERCULOUS MYCOBACTERIAL
which suggests a neoplasm. Included among these granuloma-
tous diseases are tuberculous and nontuberculous mycobacte-
DISEASE
rial diseases, actinomycosis, cat-scratch disease (CSD), and Nontuberculous mycobacteria (NTM) have become an increas-
toxoplasmosis. ingly important disease pathogen of childhood. In fact, more
than 92% of mycobacterial cervicofacial infections in children
are a result of NTM.70 The disease mainly affects children
TUBERCULOUS MYCOBACTERIAL DISEASE younger than 5 years of age, and most cases occur between 2
The most common manifestation of Mycobacterium tuberculosis and 5 years of age and in immunocompromised patients.34
infection in the head and neck is cervical lymphadenopathy. The specific organisms most commonly classified as NTM
The diagnosis of mycobacterial infections has become more are Mycobacterium kansasii, M. scrofulaceum, and M. avium-
frequent secondary to an increase in resistant strains, immigra- intracellulare. Infection by M. bovis has decreased dramatically
tion from endemic nations, and the HIV epidemic.49,78 About with the institution of milk pasteurization. These organisms are
20% of tuberculosis (TB) is extrapulmonary. However, primary commonly found in soil, water, domestic and wild animals,
salivary gland TB is rare and involves the parotid gland.60 The milk, and other food items.83 The portal of entry is believed to
diagnosis of mycobacterial infection of the salivary glands is be through the mouth, and the tonsils have been implicated in
difficult, because the differential diagnosis must include the particular.
usual spectrum of inflammatory and neoplastic diseases and The typical clinical presentation is of a rapidly enlarging and
lesions unique to the salivary glands as well as the varied clinical persistent parotid or neck mass that has failed to respond to
presentations of salivary TB. antibiotic therapy in a pediatric patient (Fig. 85-11). The skin
Tuberculous salivary gland infection is most common in becomes adherent to the surrounding tissues and develops a
older children and adults. The disease is spread by close person- characteristic violaceous discoloration. The infection might
to-person contact. Primary salivary gland infection is believed progress to fluctuation and the development of a draining
to evolve from a focus in the tonsil or gingivobuccal sulcus sinus. These lesions generally produce few systemic symptoms.
before ascending to the glands by way of their ducts. As men- Associated cervical lymphadenopathy is more commonly uni-
tioned previously, such primary TB infections occur within the lateral and is located in the high jugular nodes or preauricular
parotid gland. This infection may then spread to the cervical areas.84 The differential diagnosis should include all diseases
nodes through the lymphatic drainage.69 Other mechanisms specific to the salivary glands in addition to other granuloma-
include ascending lymphogenous spread from an infected cer- tous diseases, acute bacterial or viral infection, and malignancy.
vical lymph node and hematogenous spread from a distant Chest radiography findings are typically absent, whereas
focus.71 Mycobacteria are encapsulated in the intraglandular contrast-enhanced CT images show asymmetric cervical lymph-
lymph nodes and might be reactivated many years after the adenopathy with contiguous low-density, necrotic, ring-
acute pulmonary infection. The submandibular gland is the enhancing masses that involve the subcutaneous fat and skin.
more commonly involved gland after systemic TB infection.79 In addition, inflammatory stranding of the subcutaneous fat

the development of multiple draining cutaneous fistulae is

quite common.88 Facial nerve involvement has not been
described. A history of recent dental disease and manipula-
tion is common. Constitutional symptoms, malaise, leukocyto-
sis, and lymphadenopathy are typically absent. CT scans
typically demonstrate obliteration of the normal tissue planes
and extensive soft tissue destruction.84
Anaerobic cultures are obtained for species identification
and to confirm the diagnosis; however, the recovery rate in
culture is less than 50%.88 Diagnosis is facilitated by needle
aspiration of the mass or a fistula swab with smears and stains
to examine for the presence of sulfur granules and pathogenic
organisms. Sulfur granules have also been described for nocar-
diosis, but their identification in the presence of filamentous
gram-positive rods is diagnostic for actinomycosis.40 Biopsy
specimens show firm fibrous encasement of multiloculated
abscesses that contain a whitish-yellow purulent discharge.
Antimicrobial therapy should consist of a 6-week parenteral
FIGURE 85-11. A 4-year-old girl with nontuberculous mycobacterial course followed by an additional 6 months of oral management
involvement of periparotid lymph nodes. to completely eradicate the organism. The antimicrobial of
choice is still penicillin, because Actinomyces species are not
characteristic of bacterial inflammation is minimal or absent known to be resistant to penicillin. Other acceptable alterna-
with NTM infection.85 tives include clindamycin, doxycycline, or erythromycin.88 Sur-
Recently, numerous approaches have been described to gical excision is necessary to remove extensive fibrosis and sinus
diagnose an NTM infection. FNA biopsy is one method, but it tracts in patients who show a poor response to antibiotics and
does carry the risk of fistula formation. Purified protein deriva- for diagnosis. Response to management is generally favorable,
tive skin testing might be negative; however, NTM-specific anti- and cure rates approach 90% despite a delayed diagnosis in
gens have been developed and are reported to be extremely most instances.89
successful for diagnosis. Newer methods that use PCR tech-
niques to detect mycobacterial RNA in tissue and M. avium-
intracellulare DNA in gastric aspirates are still not widely
CAT-SCRATCH DISEASE
available.86 Traditional culture of NTM might take up to 6 Cat-scratch disease (CSD) is a granulomatous lymphadenitis
weeks and is frequently negative. that most commonly results from cutaneous inoculation caused
Medical treatment of NTM with prolonged courses of anti- by scratch trauma from a domestic cat. The causative organism
microbials, such as clarithromycin, has been advocated but is is classified as Bartonella henselae, a gram-negative intracellular
not well established. The treatment of choice is complete surgi- bacillus. Approximately 90% of patients who have CSD report
cal excision of the involved salivary gland and nodes.84,86 a history of exposure to cats, and 75% of these patients have
experienced a cat scratch or bite. Dogs have been implicated
in 5% of CSD cases. CSD affects approximately 22,000 people
OTHER GRANULOMATOUS annually and results in hospitalization of approximately 2000
DISEASES people each year in the United States.
ACTINOMYCOSIS The head and neck is the second most common site for CSD
after the upper extremity.90 The reservoir for B. henselae has
Actinomycosis is an infectious disease caused by the Actinomyces been shown to be kittens. The major vector by which cats them-
species, a gram-positive, anaerobic, non–acid-fast bacillus. His- selves are believed to become infected is the cat flea.91 The
tologically, Actinomyces bacilli have a branching, filamentous typical history is of a papule or pustule at a scratch or bite site
appearance and are similar in appearance and pathogenicity followed in 1 to 2 weeks by the development of lymphadenopa-
to mycobacteria and fungi. They are a normal commensal thy in the region of inoculation. The nodes will slowly enlarge
organism found in high concentrations in the tonsils and over a period of 1 to 2 weeks and might not resolve for 2 to 3
carious teeth. Actinomyces israelii is the most commonly encoun- months. Erythema and pain of the involved nodes with sponta-
tered species, with the balance of cases attributable to A. bovis neous suppuration will occur in a reported 10% to 30% of
and A. naeslundii. The three major clinical infections caused by patients.92,93 Fever and mild systemic symptoms might occur in
Actinomyces are cervicofacial (55%), abdominopelvic (20%), up to one third of patients. In the head and neck, this most
and pulmonothoracic (15%).72 commonly occurs in the submandibular and cervical areas;
In most cases, poor oral hygiene combined with trauma to however, preauricular adenopathy might be confused with a
the mucosa permits invasion of the organism, which leads to a parotid neoplasm.
slowly progressive inflammatory reaction. Diabetes, immune The diagnosis of CSD has changed with advances in sero-
suppression, long-term steroid use, and malnutrition have also logic and molecular biology techniques, and these methods
been implicated as predisposing factors. have replaced the need for skin testing. Testing for the pres-
Isolated salivary gland involvement probably occurs by ence of antibodies to B. henselae is now the most commonly used
means of retrograde ductal migration and primarily affects test to confirm the diagnosis.93 The two methods used for anti-
the parotid gland.87 Involvement of the salivary glands body detection are the indirect fluorescent antibody test and
also can occur as part of direct spread of an invasive cervico- the enzyme immunoassay. The test with the greatest sensitivity
facial infection. Patients typically have a painless, indurated is a Bartonella PCR hybridization assay with an aspirate or biopsy
enlargement of the involved gland that might suggest a neo- specimen, although this test might not be as easily available as
plasm. A chronic purulent drainage might occur with granu- the antibody detection techniques.44 If tissue is removed for
lomatous involvement and spread to adjacent tissue. The diagnosis, histologic examination might demonstrate B. hense-
periphery of the lesion is densely fibrotic and avascular, and lae bacilli with the use of Warthin-Starry silver staining. Lymph

node involvement shows reticular cell hyperplasia, granuloma offal infected with hydatid cysts. Humans are intermediate
formation, and widening of arteriolar walls. In more advanced hosts and are infected via the fecal-oral route by ingestion of
stages, stellate areas of necrosis coalesce to form multiple eggs. After ingestion, the worm travels from the intestine to the
microabscesses. Bartonella is a slow-growing organism, and liver via portal circulation. Occasionally, the worm can migrate
culture requires a 6-week incubation period. from the liver to other organs and possibly the salivary glands,
Atypical presentations of CSD in the head and neck have where a hydatid cyst slowly and asymptomatically develops.
been reported. Parinaud oculoglandular syndrome is a unilat- Imaging methods include ultrasonography and plain films, and
eral granulomatous conjunctivitis associated with a preauricu- ultrasonography confirms edema consistent with cyst forma-
lar or submandibular lymph node on the affected side. In tion.34 Diagnosis is made by viewing histopathologic specimens.
addition, a report of diffuse parotid enlargement with facial Care must be taken to avoid rupturing the cyst intraoperatively,
nerve palsy secondary to CSD has been described.94 Other atypi- because doing so can result in anaphylactic shock. This com-
cal presentations include vertebral osteomyelitis encephalitis, plication can be minimized by using proper technique and with
granulomatous hepatitis, and optic neuritis. In immunocom- preoperative administration of corticosteroids.34
promised patients, systemic B. henselae infection might result in
cutaneous proliferative vascular lesions similar to bacillary
angiomatosis. NONINFECTIOUS INFLAMMATORY
In most cases, no active therapy is required. The patient DISEASES OF THE SALIVARY
should be reassured that the lymphadenopathy is self-limited
and usually will resolve spontaneously in 2 to 4 months.
GLANDS
However, in patients who are systemically ill or highly symptom- Noninfectious inflammatory diseases include Sjögren syndrome,
atic, antibiotic therapy is recommended. The β-lactam antibiot- sarcoidosis, systemic lupus erythematosus, Kimura disease,
ics are ineffective in the treatment of CSD. The antibiotics Rosai-Dorfman disease, and radiation-induced sialadenitis.
reported to be most effective are rifampin, erythromycin,
gentamycin, azithromycin, and ciprofloxacin.93
SJÖGREN SYNDROME
Sjögren syndrome is a chronic autoimmune disorder of the
TOXOPLASMOSIS exocrine glands that can be systemic with involvement of
Toxoplasmosis, an uncommon disease in the United States, is multiple glands; however, the salivary and lacrimal glands are
caused by the organism Toxoplasma gondii. The usual host for primarily affected. The disease is characterized by a lympho-
this organism is the domestic cat. Parotid gland disease might plasmacytic infiltration with resulting glandular hypofunction
involve singular or multiple intraparotid or periparotid lymph that leads to dryness of the mouth and eyes.97 Sjögren syndrome
nodes. The organism exists in trophozoite, cyst, and oocyst can have a variable clinical presentation. When confined to the
forms, although the latter only exists in the feline vector. Tro- exocrine glands, it is termed primary Sjögren syndrome. The term
phozoites and cysts gain entrance to the human host most often secondary Sjögren syndrome refers to the disease in patients who
through ingestion of infected and undercooked lamb, beef, or have the characteristic signs and symptoms of primary Sjögren
chicken, or, less commonly, through cat feces. Digestion of the syndrome associated with another autoimmune disease such as
cyst capsule permits widespread hematogenous dissemination systemic lupus erythematosus, rheumatoid arthritis, or sclero-
and multiplication of trophozoites in virtually all lymphoreticu- derma. The disease might even evolve into a malignant lym-
lar organs. phoid process. The estimated prevalence of Sjögren syndrome
Both disseminated and lymphadenopathic forms of the is believed to be 1% to 3%. The disease most commonly is seen
disease have been described. Immunocompromised individu- in patients during their fourth to fifth decades of life, and more
als are most at risk for the disseminated form of the disease, than 90% of patients are women.98
which features myalgia, lethargy, and anorexia combined The etiology of Sjögren syndrome is uncertain but is believed
with hepatosplenomegaly, pericarditis, and myocarditis. Alter- to involve an interaction between a patient’s genetics, immune
nately, the lymphadenopathic variety occurs much more com- system, and environmental exposures. Genetic factors that
monly, and most patients are seen with isolated cervical involve the major histocompatibility complex and a certain
lymphadenopathy.95 group of its alleles, such as human leukocyte antigens B8 and
Definitive diagnosis can only rarely be provided by isolation DR3, are believed to create a predisposition for Sjögren syn-
of the organism. However, histopathologic findings in affected drome.97 These patients are susceptible to an initial, inciting
lymph nodes are characteristic. The lymph node architecture environmental event, most likely a viral infection that results in
is preserved, with hyperplastic follicles and germinal centers an aberrant autoimmune reaction. This autoimmune reaction
showing abundant mitoses and necrotic nuclear debris. Epithe- leads to a dense lymphocytic infiltration of the exocrine glands
lioid cells with abundant pale eosinophilic cytoplasm occur and to the production of multiple autoantibodies. Two distinct
singly or in groups and are found in cortical and paracortical autoantibodies found in Sjögren syndrome (SS) are two ribo-
zones and sinuses.80 Confirmation of a presumptive histologic nuclear proteins known as Ro (or SS-A) and La (or SS-B). The
diagnosis is made by acute and convalescent serologic testing. presence of these antibodies is used to assist in establishing the
Chemotherapy is generally reserved for obviously progressive diagnosis of Sjögren syndrome.98 Immunologic pathogenesis is
infections or for those that involve pregnant or immunocom- related to the overstimulation of B cells that results in an excess
promised individuals, and it consists of the combined adminis- of immunoglobulins and autoantibodies, which alters the distri-
tration of pyrimethamine and trisulfapyrimidines. bution of B cells both peripherally and in salivary glands. This
disruption results in the formation of germinal centers, which
enables autoreactive B-cell clones to escape tolerance check-
PARASITIC SALIVARY GLAND points, thereby selecting for autoreactive B cells. Additionally,
follicular helper T-cell levels are increased and seem to play a
INFECTIONS role in the development of Sjögren syndrome.99
Hydatid disease of the parotid gland is extremely rare, and the The predominant clinical presentation of Sjögren syndrome
organism responsible is Echinococcus granulosus.96 Dogs are the is dryness of the mouth and eyes. Xerostomia results in difficulty
primary host and acquire the organism by consuming uncooked chewing and swallowing food, difficulty with phonation, dental

caries, and adherence of food to the buccal mucosa. Intolerance of patients.98 Most commonly, the vasculitis manifests itself in
to acidic and spicy foods is also a common complaint. The most the skin in the form of Raynaud phenomenon and recurrent
common ocular complaint is a foreign body sensation in the urticaria-like lesions. Central nervous system involvement is
eye, which is commonly described as “gritty” or “sandy.” Chronic also reported to occur in Sjögren syndrome, and neurologic
irritation and destruction of the corneal and conjunctival epi- involvement includes peripheral sensory and motor polyneu-
thelium results in keratoconjunctivitis sicca. ropathies that can mimic multiple sclerosis.
The physical examination of patients with Sjögren syndrome Sjögren syndrome also predisposes patients to the develop-
can vary. Overt signs of this syndrome consist of dry oral ment of malignant lymphoproliferative disorders. The increased
mucosal surfaces, multiple dental caries, and the absence of risk for lymphoma in patients with Sjögren syndrome extends
pooled saliva in the floor of the mouth. The tongue is typically even after two decades of a benign disease course. Patients
smooth with fissures and atrophy of the filiform papillae. with persistent unilateral or bilateral parotid gland enlarge-
Patients with Sjögren syndrome also commonly have an intra- ment are at higher risk for the development of lymphoma. The
oral fungal overgrowth with Candida albicans. The examination pathogenesis of lymphoma secondary to primary Sjögren syn-
of the salivary glands results in the expression of scant or cloudy drome is thought to be due to the chronic overstimulation of
saliva from the ducts. Salivary gland enlargement, most com- B cells.101
monly in the parotid glands, occurs in 25% to 66% of patients. In addition to the clinical examination, establishing the
This might begin unilaterally, but most patients eventually presence of an autoimmune process is mandated for the diag-
develop bilateral enlargement, which may be recurrent and nosis of Sjögren syndrome; this can be done by detecting the
episodic or chronic and fixed (Fig. 85-12). Objective evaluation presence of autoantibodies and by minor salivary gland biopsy.
of salivary flow rate can be performed with Lashley cups that Testing for autoantibodies to the ribonuclear proteins Ro
fit over the opening of the Stensen duct and collect saliva. (SS-A) and La (SS-B) is done by use of an enzyme-linked immu-
Sialography demonstrates sialectasis in 85% to 97% of patients nosorbent assay. The biopsy of labial accessory salivary glands
with Sjögren syndrome.30 that demonstrate salivary gland disease is one of the most con-
The ocular findings in patients with Sjögren syndrome sistent features of primary Sjögren syndrome. The biopsy
include dilatation of the bulbar conjunctival vessels, pericor- should include several glandular lobes obtained from areas
neal injection, irregularity of the corneal image, and occasion- with normal overlying mucosa to exclude nonspecific inflam-
ally enlargement of the lacrimal gland. The tear secretion rate matory findings.97 The histopathologic lesion is a lymphocytic
may be assessed by means of a Schirmer test. In addition, stain- infiltrate that produces a chronic focal sialadenitis. More spe-
ing of damaged corneal and conjunctival epithelia by Rose cifically, the lesion consists of multiple focal mononuclear
Bengal dye is reported to be more specific for keratoconjunc- aggregates that are adjacent to and replace the normal acini.
tivitis sicca.100 Several histologic classification methods have been devised that
The systemic nature of Sjögren syndrome might result in a score the number of inflammatory foci seen on salivary gland
wide variety of findings other than dryness of the mouth and biopsy.
eyes. Systemic manifestations include generalized malaise, low- Several sets of diagnostic criteria that encompass findings
grade fever, myalgia, and arthralgia. Dryness of the pharynx on history, physical examination, and laboratory testing have
and esophagus results in dysphagia, and involvement of the been proposed for the diagnosis of Sjögren syndrome. In
tracheobronchial system might lead to bronchitis or pneumo- general, the diagnosis consists of establishing the presence of
nia. The renal system may also be affected, resulting in renal keratoconjunctivitis sicca and xerostomia by means of clinical
tubular acidosis. Vasculitis is reported to occur in 20% to 30% examination and objective testing. This testing should include
objective measurements of decreased salivary and tear flow
along with a minor salivary gland biopsy. In addition, laboratory
evidence suggestive of a systemic autoimmune disease, specifi-
cally against SS-A and SS-B ribonuclear proteins, is necessary
for the diagnosis of Sjögren syndrome.98 Laboratory evaluation
that includes assessment for the presence of autoantibodies and
B-cell subset analysis should be performed.99 Patients who have
objective signs of sicca complex but no evidence of an autoim-
mune process should be evaluated for other causes, such as HIV
or hepatitis C virus infections.
Multiple factors must be considered in the differential diag-
nosis of patients being evaluated for Sjögren syndrome. A
patient’s general state of hydration and the presence of sys-
temic conditions such as diabetes and cystic fibrosis should be
assessed. One of the most common causes of xerostomia is
medications. Sedatives, antipsychotics, antidepressants, antihis-
tamines, and diuretics are the classes of drugs most often associ-
ated with oral dryness. Salivary gland exposure to therapeutic
irradiation greater than 4000 cGy will result in severe and per-
manent secretory hypofunction.100
The salivary gland enlargement frequently found in Sjögren
syndrome may also be caused by several other conditions. Uni-
lateral salivary gland enlargement despite an established diag-
nosis of Sjögren syndrome should raise the suspicion of tumor.30
The treatment of Sjögren syndrome involves symptomatic
treatment and prevention of irreversible damage to the teeth
and eyes. The management of the oral component involves
FIGURE 85-12. Bilateral parotid gland enlargement in a middle-aged increasing the secretion rate of remaining salivary glands, using
woman with Sjögren syndrome. saliva substitutes, treating and preventing dental caries, and

eradicating fungal overgrowth.33 Stimulation of residual salivary The diagnosis of sarcoidosis is based on clinical presentation,
gland function might be accomplished by local methods, such radiographic findings, and biopsy of noncaseating granuloma.
as chewing sugarless gum or candies. The muscarinic- Additional laboratory findings of a CD4/CD8 T-lymphocyte
cholinergic agonist pilocarpine is the most commonly used ratio greater than 3.5 in a bronchoalveolar lavage and a soluble
systemic sialogogue. The drug is administered in 5-mg doses angiotensin-converting enzyme level more than twice the
three to four times daily; however, side effects such as sweating, normal value support the diagnosis of sarcoidosis. A commonly
flushing, and increased urination are common. Because preferred biopsy site is the lip mucosa. Labial salivary gland
primary Sjögren syndrome is thought to arise from chronic biopsy in conjunction with anti-AA amyloid antibody immuno
stimulation of B cells, multiple studies have been performed to staining is an effective method for diagnosing secondary amy-
assess the efficacy of B-cell depletion therapies. Rituximab, a loidosis. Labial salivary gland biopsy shows periductal amyloid
monoclonal antibody to CD20, shows depletion in both periph- deposits, and anti-AA amyloid immunostaining reveals amyloid
eral blood B-cell subsets and salivary gland B cells. Therefore deposits around acini.106 Corticosteroids are the primary treat-
B-cell depletion improves both local and systemic symptoms of ment for parotid involvement of sarcoidosis, and the lowest
Sjögren syndrome such as xerostomia, fatigue, joint tenderness, effective dosage should be used. In some patients, the disease
and so on.21 Dental treatment with fluoride is used to prevent may resolve spontaneously.101
and control dental caries. The treatment for keratoconjuncti-
vitis consists of the use of commercially available eye lubricants
and eye patching if corneal ulceration develops. The use of
KIMURA DISEASE
systemic corticosteroids or cytotoxic drugs is reserved for the Kimura disease is a chronic inflammatory disease that often
severe extraglandular complications such as glomerulonephri- manifests with painless and diffuse soft tissue swelling in the
tis or necrotizing vasculitis.97 cervicofacial region.107 Patients usually come to medical atten-
Patients with recurrent sialadenitis may benefit from sialen- tion with a slow-growing mass in the neck and retroauricular
doscopy to dilate and wash out the affected ducts. A multidis- areas, with pruritis overlying the nodular areas.108 Even though
ciplinary approach that involves the salivary endoscopist, who parotid involvement is uncommon, it can be present as a uni-
can offer interval procedures, and the rheumatologist can help lateral or bilateral mass; unilateral involvement is more
optimize treatment in patients who come to medical attention common.84,86 Lymph nodes are characterized by eosinophilic
with predominantly salivary symptoms. My experience is that in microabscesses, eosinophilic folliculolysis, perivenular sclerosis,
these cases, sialendoscopy can offer a method of reducing the and eosinophilic infiltrates in the germinal center; however,
intensity and frequency of symptoms and may make the patient lymph node architecture is maintained. Asian men in the third
amenable to low-intensity medical therapy that has fewer decade of life are most commonly affected, but other races,
serious side effects. If treatments fail, gland excision for relief genders, and ages should not be excluded.84 Laboratory evalu-
of symptoms may be indicated. ation commonly shows peripheral blood eosinophilia and ele-
vated serum immunoglobulin E.109 Blood eosinophilia is related
to the mass size and may be used to measure disease activity.55,88
SARCOIDOSIS Although no standard therapy has been established, treatment
Sarcoidosis involves the formation of immune granulomas in options for Kimura disease include observation, surgery, or
various organs, especially in the lungs and lymphatic organs. It radiotherapy or medications such as antihistamines (cetiri-
commonly affects adults within the second to fourth decades zine), steroids, and cyclosporine.110,111
of life. Although the etiology is unknown, it is thought that
antigens are triggered by an environmental or infectious
event.101 Incidence is slightly higher in women (1.3%) than
ROSAI-DORFMAN DISEASE
men (1%), and blacks (2.4%) have a higher incidence than The most common presentation of Rosai-Dorfman disease is
whites (0.8%).102 Common symptoms include a persistent dry bilateral, painless cervical lymphadenopathy.112,113 Salivary
cough, eye or skin manifestations, peripheral lymph node gland involvement has been observed in approximately 30%
enlargement, fatigue, weight loss, fever or night sweats, and of cases, and common imaging findings include lymphoid
erythema nodosum.103 Laboratory evaluation can show hyper- hyperplasia in the parotid gland adjacent to the submandibular
calcemia and abnormal metabolism of vitamin D3 within granu- gland or diffuse enlargement of the submandibular glands.
lomatous lesions. Imaging shows abnormal chest radiography Management of Rosai-Dorfman disease includes observation,
in 90% of cases. Furthermore, lymphadenopathy and pulmo- radiation therapy, chemotherapy, steroids, and surgery.93 Labo-
nary infiltrates may also be present.104 ratory evaluation shows immunohistochemical staining that is
Sarcoidosis that involves the salivary glands is seen in 5% to positive for S-100 protein and immunoreactivity against α-1–
10% of cases and has a variety of presentations. Three patterns antichymotrypsin, CD68, and MAC387 antibodies.94
of presentation are common, the first and most common of
which involves major salivary gland swelling. If xerostomia is
evident, it is directly proportional to the amount of granuloma-
tous infiltration. The second presentation does not involve sali-
SUMMARY
vary gland edema; however, noncaseating granulomas are Salivary gland inflammation is most commonly due to obstruc-
apparent upon biopsy of minor salivary glands. The third tion of salivary outflow by a sialolith in the duct and/or a
pattern includes uvoparotid fever, or Heerfordt syndrome, a bacterial infection. Conservative medical therapy for acute
chronic febrile enlargement of the parotid glands along with infections and minimally invasive procedures such as sialen-
uveitis and facial nerve palsy.101 When sarcoidosis affects major doscopy for chronic inflammation are usually effective
salivary glands, it is characterized by a chronic, painless parotid enough to spare the patient an incision into the duct or
enlargement spread throughout the gland.60 Salivary gland gland removal. Bacterial infections are acutely symptomatic
involvement is uncommon and is present bilaterally in 30% to and tend to occur in dehydrated or debilitated patients, such
70% of patients.105 Laboratory evaluation commonly shows as hospitalized elderly patients following surgery. Virus-
an elevated erythrocyte sedimentation rate. Additionally, induced salivary gland inflammation can include mild dis-
anemia, leukopenia, eosinophilia, and hypercalcemia may also eases such as mumps to more severe pathologies such as HIV,
be present. which leads to bilateral, recurrent BLECs. Granulomatous

diseases, which typically manifest as a painless enlarging mass, Lampropoulos P, Rizos S, Marinis A: Acute suppurative parotitis: a
tend to affect mostly children and the elderly. dreadful complication in elderly surgical patients. Surg Infect (Larchmt)
13(4):266–269, 2012.
Luers JC, Grosheva M, Reifferscheid V, et al: Sialendoscopy for sialoli-
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Inflammatory Disorders of The Salivary Glands

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Inflammatory Disorders of The Salivary Glands

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Inflammatory Disorders of 85

the Salivary Glands

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Patients with sialolithiasis are seen with recurrent episodes

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shown to induce parotid swelling; this is due to protease inhibi-

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the development of multiple draining cutaneous fistulae is

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