Inflammatory Disorders of the Salivary Glands

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CHAPTER 86 Inflammatory Disorders of the Salivary Glands

Key Points

Salivary gland infections and inflammations have a wide range of presentations, depending on the etiologic agents involved and the chronicity of the infection. These might range from acute localized infections like bacterial sialadenitis to systemic diseases caused by viruses such as the paramyxovirus or the human immunodeficiency virus (HIV). Noninfectious inflammations such as Sjögren’s syndrome may present as a chronic swelling of the salivary glands.

Bacterial Infection of the Salivary Glands

Acute Suppurative Sialadenitis

Acute sialadenitis is a bacterial inflammation of the salivary glands. Although these infections occur in all major salivary glands, the parotid gland is most commonly involved. Frequently associated with medically debilitated and postoperative patients, the incidence of acute sialadenitis is approximately 0.02% of hospital admissions. It occurs between 1 in 1000 and 1 in 2000 operative procedures.1 Patients undergoing major abdominal and hip repair surgery have been identified as being at increased risk for acute suppurative sialadenitis. The disease is most commonly reported to occur within the first 2 postoperative weeks.2 Of the medically ill patients affected by sialadenitis, approximately 25% have a malignant lesion and another 50% have a preexisting infection elsewhere than the head and neck. Most affected patients are between 50 and 60 years of age, with an equal incidence among men and women.3

Acute infection of the salivary glands is caused by retrograde bacterial contamination of the salivary ducts from the oral cavity. Stasis of salivary flow secondary to dehydration or significant hemorrhage permits retrograde migration of bacteria, producing suppurative infection of the gland parenchyma. The parotid gland is most susceptible to such infections.

In contrast to the mainly serous saliva produced by the parotid gland, the saliva made by the submandibular and sublingual glands is primarily mucoid. Serous saliva, unlike mucinous saliva, is deficient in lysosomes, IgA antibodies, and sialic acid, which have antimicrobial properties. In addition, the saliva from the submandibular and sublingual glands contains high-molecular-weight glycoproteins that competitively inhibit bacterial attachment to the epithelial cells of the salivary ducts.4 Several predisposing factors might lead to acute sialadenitis. These include diseases such as diabetes mellitus, periodontal disease, hypothyroidism, renal failure, and Sjögren’s syndrome. Medications might produce reduced salivary flow through multiple mechanisms (Fig. 86-1).

Mechanical impairment of salivary flow also predisposes to acute infection. Stenosis of the salivary ducts secondary to trauma or a foreign body has been reported to result in acute sialadenitis. Sialolithiasis, more frequent in the ducts of the submandibular and sublingual glands, may also contribute to acute infection but more commonly produces chronic salivary gland infection.5 The most commonly cultured organism among hospitalized patients with acute sialadenitis is penicillin-resistant Staphylococcus aureus, which is responsible for 50% to 90% of cases. In addition, Streptococcus species including Streptococcus pyogenes, Streptococcus viridans, and Streptococcus pneumoniae, as well as Hemophilus influenzae, can be isolated in community-acquired cases. More recently, the importance of anaerobic and gram-negative bacteria in acute suppurative parotitis has been established. In one study, anaerobic bacteria were isolated from 64% of cases of acute suppurative sialadenitis. The anaerobic bacteria most frequently cultured were Peptostreptococcus, bacteroides species, Prevotella species, and fusobacterium. In Southeast Asia, Burkholderia pseudomallei is a common cause of parotitis. This apparent shift in microbiology might be the result of improved anaerobic bacterial culture technique rather than a true change in the flora of acute salivary gland infections.3,6,7

Acute suppurative sialadenitis presents with local symptoms consisting of rapid onset of pain and swelling over the affected salivary gland (Fig. 86-2). Systemic manifestations include fever, chills, and malaise. Importantly, one should review the medical and surgical history for the previously noted risk factors that would make a patient more susceptible to acute salivary gland infection. On physical examination the patient might demonstrate signs of systemic dehydration with dry mucous membranes. Local findings include tenderness to palpation, with warmth and induration of the overlying skin. Bimanual palpation of the gland results in suppurative discharge from the duct orifice in approximately three fourths of cases (Fig. 86-3).2 Although typically limited to one gland, multiple glands might be affected, with a reported incidence of bilateral involvement of up to 25% of cases.8

The laboratory evaluation will reveal a leukocytosis with neutrophilia. Generally, the serum amylase is normal. Imaging of the affected gland with computed tomography (CT) or ultrasound (US) for abscess formation is indicated in patients who do not respond to medical therapy within 48 to 72 hours. Sialography performed in the acute phases of sialadenitis provides little useful information and is contraindicated because it can exacerbate the existing inflammation. Magnetic resonance imaging (MRI) may be used to evaluate the salivary duct architecture noninvasively; however, its usefulness in acute infection has yet to be established.

Cultures of purulent drainage from the duct orifice should be obtained. Recent reports advocate the use of percutaneous needle aspiration of the involved duct. This technique limits the amount of contamination encountered by means of an intraoral culture.6,9

Although the diagnosis of acute parotitis is usually apparent, nonparotid swelling can mimic parotitis. Such conditions include lymphoma, lymphangitis external otitis, Bezold’s abscess, cervical adenitis, dental abscesses presenting as buccal or masseteric space abscesses, and infected branchial cleft or sebaceous cysts.10

Initial treatment of acute suppurative sialadenitis begins with aggressive medical management. This includes prompt fluid and electrolyte replacement, oral hygiene, reversal of salivary stasis, and antimicrobial therapy. Stimulation of salivary flow is accomplished by the use of sialogogues such as lemon drops and orange juice. Antisialogogic medications should be discontinued. In addition, capable patients should be instructed on regular external and bimanual massage, starting from the distal bed of the gland and working in the direction of duct drainage. Analgesics and local heat application ease the discomfort. If neither saliva nor pus can be expressed from the duct, cannulation and serial dilation may be necessary to establish patency.

Antimicrobial therapy is an essential part of the management of acute salivary gland infections. Antimicrobial therapy is initiated empirically toward gram-positive and anaerobic bacteria. However, the recovery of β-lactamase–producing bacteria in 75% of patients requires the use of augmented penicillin and antistaphylococcal penicillin or a first-generation cephalosporin.6,11 The use of clindamycin or the addition of metronidazole to the first-line agents to broaden anaerobic coverage has been advocated by some authors.6 In patients from nursing home environments or cases of nosocomial infection, empiric vancomycin has been advocated given the prevalence of methicillin-resistant S. aureus. Aminoglycosides have also been proposed by some in the treatment of critically ill patients. Culture results should be used to further direct antimicrobial treatment. Response to antimicrobial therapy is seen within 48 to 72 hours of initiating treatment and should continue for 1 week after resolution of symptoms.1

Rarely, conservative measures fail to eradicate the infection, and surgical drainage of a loculated abscess is necessary. The surgical approach involves elevation of an anterior-based facial flap with abscess drainage by way of radial incisions in the parotid fascia parallel to the facial nerve branches. A drain should be placed, and the wound edges should be loosely approximated, with the central aspect left to heal by secondary intention (Fig. 86-4).

Complications of acute suppurative parotitis are unusual. Suppuration confined to the duct lumen might eventually erode through the epithelium into the interstices of the parenchyma, creating multiple small abscesses that might coalesce into larger collections that can infiltrate a number of potential spaces of the neck. Osteomyelitis of the mandible and temporomandibular joint, thrombophlebitis of the jugular vein, septicemia, respiratory obstruction, and death are potential sequelae of suppurative parotitis. Rupture through the floor of the external auditory canal, spontaneous drainage through the cheek, and extension to the face, neck, and mediastinum have also been reported (Fig. 86-5).12,13 Facial nerve paralysis, whether complete or incomplete, is uncommon. The etiology of paralysis is unknown but is thought to be due to the virulence of the offending organisms, perineuritis, or acute nerve compression. Because facial nerve paralysis is highly suggestive of parotid malignancy, all patients with paralysis should be followed until the inflammatory process has resolved and facial nerve function returned.14 Acute suppurative sialadenitis is associated with 20% to 40% reported mortality; however, the prognosis is primarily related to the medical condition of the patient.2

Recurrent Parotitis of Childhood

Recurrent parotitis of childhood (RPC) is an uncommon inflammatory condition of the parotid gland characterized by periodic episodes of swelling and pain. It can be distinguished from suppurative parotitis by the inability to express pus from the parotid duct. The age of onset ranges from 8 months to 16 years, with a reported peak incidence between the ages of 3 and 6 years.17,18 Boys are more frequently affected than girls.

The cause of recurrent parotitis of childhood remains unknown, and multiple etiologies have been proposed. Several authors advocate that congenital ectasia of portions of the secondary ductal system predisposes children for bacterial colonization leading to recurrent parotitis.17 S. aureus and S. viridans are the most commonly isolated organisms from the parotid ducts of patients. A familial form of RPC has been described with autosomal inheritance.19 Immunologic abnormalities with isolated IgG3 and IgA deficiencies have been associated with recurrent parotitis. In addition, parotid swelling might be the sole manifestation of juvenile-onset primary Sjögren’s syndrome. Several viruses might also play a role in RPC. A history of mumps parotitis often exists. Repeated multiplication of the Epstein-Barr virus in the parotid gland might be responsible for establishing repeated parotid gland inflammation, and RPC has a reported incidence of 20% in HIV-infected children.20,21

The histologic appearance of affected parotid glands demonstrates massive periductal lymphocytic infiltration. The intraglandular ducts are dilated and measure approximately 1 to 2 mm in diameter.20

Clinically, patients are seen with recurrent episodes of acute or subacute parotid gland swelling along with fever, malaise, and pain frequently after a meal. Episodes of RPC are commonly unilateral, but bilateral involvement has been reported in up to 44% of cases. Afflicted patients tend to experience exacerbations every 3 to 4 months; however, in one series with 53 patients, mean frequency was eight episodes per year. Each might last days to weeks.17 Diagnosis is usually delayed more than 1 year.

Several imaging modalities may be used to study the ductal system of patients with RPC. The characteristic finding is sialectasis, which on conventional sialography appears as numerous scattered punctate pools of contrast. US of the parotid gland reveals an enlarged gland with multiple small hypoechoic areas. These areas represent both sialectasis of the ducts and the surrounding lymphocytic infiltration. Recently, MR sialography has been reported to be useful in the evaluation of RPC.20 It is a noninvasive study, not requiring contrast, and may be used during acute episodes.

Treatment consists of adequate hydration, gland massage, local heat, sialagogues, and appropriate intravenous antibiotics. Empiric therapy before culture results should consist of a penicillinase-resistant antistaphylococcal antibiotic. In general, this will lead to rapid resolution of swelling and discomfort. Some authors have advocated prophylactic antibiotics, but this has not been proven effective. Fortunately most cases of recurring parotitis resolve spontaneously near the onset of puberty or in late adolescence, and surgical treatment is rarely required. Of the available options, parotidectomy is curative but carries the risk of facial nerve damage. Ductal ligation and tympanic neurectomy have been reported but with varying results.

Chronic Sialadenitis

Chronic sialadenitis is a localized condition of the salivary gland characterized by repeated episodes of pain and inflammation. The parotid gland is the most frequently affected site.22 The initial inciting factor is believed to be salivary duct obstruction, with resulting salivary stasis. The most common cause of ductal obstruction is sialolithiasis. Stricture of the salivary duct, extrinsic compression by tumor, stenosis secondary to scar in adjacent tissue, congenital dilation, and foreign body are additional causes of duct obstruction.23 Salivary stasis from obstruction predisposes patients to episodes of infection and inflammation. Recurrent inflammatory reactions result in progressive acinar destruction with fibrous replacement and sialectasis (Fig. 86-6).

Clinically, patients are seen with a history of recurrent swelling and tenderness of the affected gland associated with eating. Patients frequently report an initial episode of acute suppurative sialadenitis. Asymptomatic intervals might range from a few weeks to months. The physical examination reveals enlargement of the gland, and minimal saliva can be milked from the duct orifice.

Treatment of chronic sialadenitis can be frustrating, and no treatments are consistently successful. Tympanic neurectomy and parotid duct ligation are procedures advocated for chronic parotitis to induce atrophy of the gland, but these have failed to show reliable benefit. Surgical removal of the gland when conservative management has failed to control symptoms has been shown to be safe and effective.24

Possible complications of chronic sialadenitis include the development of a benign lymphoepithelial lesion, Kuttner’s tumor, and ductal carcinoma.2527 A benign lymphoepithelial lesion is characterized by a lymphoreticular infiltrate with acinar atrophy, irregularly placed nuclei, and ductal metaplasia. The metaplasia results in the development of epimyoepithelial islands. Women in the fifth to sixth decade of life are more commonly affected. It has been associated with Sjögren’s syndrome and has also been termed Mikulicz’s disease. A benign lymphoepithelial lesion typically presents as an asymptomatic mass. FNA may be used for diagnosis and allow for a nonsurgical approach to management.27 However, patients must be followed because there are reports of the development of malignancy from these lesions.26

Kuttner’s tumor is a benign inflammatory process similar to a benign lymphoepithelial lesion. However, the lesion occurs almost exclusively in the submandibular gland. Kuttner’s tumors are most common in middle-aged adults and present as a painless mass. Histologically, there is a heavy lymphoid infiltrate among discrete tubular structures with regularly aligned nuclei, which differentiates them from a benign lymphoepithelial lesion. Kuttner’s tumor might also be followed clinically. Again, careful and routine assessment of patients with chronic sialadenitis is underscored by reports of the development of malignancies including salivary ductal carcinoma.26


Sialolithiasis is the formation of calculi in the ductal system of the salivary glands. The submandibular gland is most commonly affected, with 80% to 90% of stones developing in Wharton’s duct. Approximately 10% to 20% of calculi form in the parotid (Stensen’s) duct and 1% in the sublingual duct.28 Patients in their fifth to eighth decade of life represent most cases. Sialolithiasis in children is rare; however, if afflicted, children most commonly are seen at 10 years of age.6 Men tend to develop calculi much more frequently than women.

Salivary stones are composed predominantly of calcium phosphate and carbonate in combination with an organic matrix of glycoproteins and mucopolysaccharides. Small amounts of other salts such as magnesium, potassium, and ammonium are also involved in stone formation.29

The exact etiology of sialolithiasis is uncertain. There does not seem to be a relationship between their formation and serum calcium or phosphorous levels.30 Salivary stasis and ductal inflammation and injury are important factors contributing to stone formation. It is believed that intermittent salivary stasis results in an alteration of the mucoid elements of saliva forming an organic gel. This gel becomes the framework for the deposition of salts, which leads to the development of calculi. The relationship between sialolithiasis and chronic sialadenitis might differ between salivary glands.28 In the submandibular gland, development of a sialolith might be the primary event that results in stagnation of saliva and inflammation, encouraging bacterial migration and resultant sialadenitis. In contrast, inflammation and ductal injury in the parotid gland from chronic sialadenitis are believed to be the inciting processes for sialolithiasis.

Several factors might account for the propensity of salivary stones to form in the submandibular gland. Wharton’s duct is longer, has a larger caliber, and is angulated against gravity as it courses around the mylohyoid muscle, all of which results in slower salivary flow rates. Also, the saliva produced by the gland itself is more viscous and has a higher calcium and phosphorous concentration.28,31

In the parotid gland, stones are most commonly located at the hilum or parenchyma. Sialolithiasis in the submandibular gland tends to develop in the duct.32

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 (Fig. 86-7). On physical examination, bimanual palpation will reveal the presence of a palpable stone in most cases involving the submandibular duct. Parotid stones might be noted at the orifice of Stensen’s duct or along the course of the duct.

Imaging of the salivary glands for sialolithiasis may be accomplished with plain radiographs, conventional and digital sialography, US, CT, and MRI. Plain radiographs that use intraoral or occlusal views might be used to identify radiopaque stones (Fig. 86-8

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