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).

Figure 86-1. Pathophysiology and predisposing factors for the development of acute and chronic suppurative sialadenitis.

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

Figure 86-2. An acutely formed abscess of the parotid gland demonstrating diffuse unilateral edema.

Figure 86-3. A purulent exudate emerging from the orifice of Stensen’s duct.

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).

Figure 86-4. Surgical approach to the drainage of an acute parotid gland abscess. A, Standard curvilinear incision. B, Elevation of an anterior-based facial flap and identification of regional anatomic landmarks. C, Abscess drainage by means of incisions in the parotid fascia parallel to facial nerve branches. D, Marginal approximation of wound edges and drainage with the central aspect left to heal by secondary intention.

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

Figure 86-5. Patterns of progression of parotid abscesses. A, Prestyloid extension to parapharyngeal space (arrow). B, Poststyloid extension to carotid sheath (arrow). C, Anteroinferior extension anterior to the posterior digastric belly of the submandibular space (arrow). D, Inferior extension posterior to the posterior digastric belly to the carotid triangle (arrow).