Parotitis
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| Mumps virus |
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Parotitis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Parotitis On the Web |
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American Roentgen Ray Society Images of Parotitis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Parotitis is an inflammatory disorder of the salivary gland, or sialadenitis. It is most commonly infectious in etiology but can be autoimmune or neoplastic.
Epidemiology and Demographics
The first report of acute bacterial sialadenitis dates back to 1828 described in a 71-year-old man whose infection progressed to gangrene. President Garfield died from acute parotitis complicating abdominal surgery. Parotitis carried an 80% mortality rate in the 1800s and remains a quite morbid infection with estimated mortality of 20-50% in the present day.
Acute infection can occur in any salivary gland but the most commonly affected one is the parotid. This is thought to be due to a combination of anatomic and physiologic factors. The saliva from the parotid is less mucoid than that from the other salivary glands. IgA, lysozyme and sialic acid are all found in smaller amounts in the more viscous parotid secretions. These substances are thought to help fight off ascending bacterial infection. Bacterial parotitis is generally unilateral in adults (75-90%), while viral is generally bilateral.
Though 80-90% of salivary calculi occur in the Wharton’s duct of the submandibular gland, the parotid remains the most common site of acute suppurative salivary infection. The secretions from the submandibular gland are more alkaline, thought to result in a higher concentration of insoluble calcium phosphate.
Pathophysiology
Parotitis is a disease that occurs in debilitated patients. Dehydration and decreased salivary flow/stasis are the main risk factors for ascending infection through Stenson’s duct to the gland. Postoperative patients who are dehydrated and NPO with little salivary stimulation are at particular risk with an incidence estimated at 1 in 1000. Debilitating medical conditions such as Diabetes mellitus, renal failure, HIV and Sjögrens’s syndrome are risk factors.
Patients with Anorexia, Bulimia, CF or those with salivary ductal dilation are also at risk. Ductal dilation is found in those with high intraoral pressure such as trumpet players and glass blowers. Medications with anticholinergic properties or diuretic effects
The most common bacterial cause is S. aureus. S. pneumonia, S. pyogenes and H. influenza are also common. Less commonly gram negative rods (GNR) as well as anaerobes are found. M. tuberculosis and T. pallidum have also been reported but are usually associated with chronic, painless infection.
Viral etiologies include paramyxovirus (particularly Mumps), influenza, parainfluenza, echovirus and coxsackie. Cytomegalovirus (CMV) and adenovirus have been implicated in HIV patients.
Nonbacterial causes include Wegener’s granulomatosis and lymphoma. Cat-scratch and actinomycosis should be considered if the patient fails to respond to standard therapy. This predispose to parotitis. [1]
Diagnosis
The diagnosis is a clinical one. Imaging is usually reserved to assess for a complication such as abscess formation, invasion of the deep neck spaces, mediastinitis, jugular vein thrombosis or osteomyelitis of the mandible. Local invasion of the temporomandibular joint (TMJ) and thrombophlebitis of the retromandibular and facial veins have also been noted. Facial nerve dysfunction is rare and usually transient if the infection is treated. More prolonged palsy suggests neoplasm. Because of the underlying debility, the most worrisome complications are systemic and sepsis can rapidly develop. Chronic recurrent parotitis can occur as a separate entity or secondary to ductal stenosis from initial infection.
Treatment
The treatment of viral parotitis is largely supportive. Bacterial parotitis is targeted toward gram positive and anaerobic organisms. 70% of those cultured are beta-lactamase producers so Augmentin is recommended. Antistaphylococcal penicillins are also advocated. Some suggest the addition of metronidazole or clindamycin. Systemic symptoms or failure to improve in 48 hrs warrants IV therapy and consideration of additional coverage for GNR. Adjunctive therapy with warm compresses, mouth irrigation, administration of sialagogues (lemon drops) and bimanual massage of the gland intraorrally and externally can be employed.
Surgery is referred for recalcitrant infections, abscess drainage and to obtain tissue if a noninfectious cause is suspected.
References
- ↑ McQuone SJ. Acute Viral and Bacterial Infections of the Salivary Glands. Otolaryngologic Clinics of North America. 1999, 32:793-811. PMID 10477787