Suppurative Parotitis

An 82-year-old woman, who was a nursing home resident, presented to the emergency department with a 1-day history of altered mental status, fever, chills, and right-sided facial redness and swelling. Her medical history included dementia, hypertension, congestive heart failure, and chronic kidney disease stage 2.

Her temperature was 38.2°C (100.7°F); respiration rate, 28 breaths per minute; and heart rate, 98 beats per minute. She was lethargic and moaning. Diffuse, flat erythema with unclear borders was noted on the right side of her face and neck. Palpation revealed a firm, tender preauricular mass without areas of fluctuation (A).

White blood cell (WBC) count was 37,600/µL (normal range, 4500 to 10,000/µL) with polymorphonuclear cells at 88%; C-reactive protein (CRP) level was 30.7 mg/dL (normal range, 0 to 1.0 mg/dL). A maxillofacial CT scan (B) confirmed right parotitis with extensive superficial and deep cellulitis.

The patient was admitted, and blood cultures were obtained. Because of a penicillin allergy, she was started on intravenous vancomycin, metronidazole, and cefepime. Blood cultures grew methicillin-resistant Staphylococcus aureus (MRSA), sensitive to vancomycin. Her WBC count and CRP level returned to normal, and her facial inflammation improved. She was discharged to her nursing home in stable condition with a 3-week course of vancomycin.

Of all the salivary glands, the parotid gland is most commonly affected by an inflammatory process. Acute bacterial parotitis is generally caused by Staphylococcus aureus, Streptococcus species, gram-negative bacteria (rarely), and anaerobic bacteria including Peptostreptococcus, Bacteroides, Porphyromonas, and Prevotella species. Risk factors include age, dehydration, intubation, poor oral hygiene, recent intensive teeth cleaning, anticholinergics and other drugs that reduce salivary flow, malnutrition, salivary calculi with obstruction, and oral cavity neoplasms.¹

Acute parotitis is characterized by the sudden onset of firm, erythematous swelling of the preauricular and postauricular areas that extends to the angle of the mandible. This is associated with localized tenderness, fever, chills, marked toxicity, trismus, and dysphagia.

The diagnosis is usually made when the characteristic clinical findings are present. When purulent drainage is present at the opening of Stensen’s duct, Gram staining and culture should be obtained. Needle aspiration of the parotid gland by extra-oral route can be considered to identify the causative organisms. The most sensitive imaging modality for abscess identification is CT.

Initial empiric antimicrobial regimens are based on the expected microbiology and host factors and should be directed against Staphylococcus aureus (including MRSA) and mixed oral aerobes and anaerobes. Additional coverage for Enterobacteriaceae and Pseudomonas should be considered in immunocompromised patients and those with recent hospitalization. The antimicrobial regimen should be narrowed once microbiologic data become available. Surgical treatment can be considered if there is no improvement after 48 hours of antibiotic therapy, facial nerve or other adjacent structure involvement, and/or abscess formation within gland parenchyma.

Complications of acute parotitis include respiratory obstruction, septicemia, facial bone osteomyelitis, septic jugular thrombophlebitis,² facial nerve palsy, fistula formation, and ductal stenosis. The prognosis varies, but resolution is likely in healthy patients who receive early aggressive treatment.

REFERENCES:

1. Brook I. Diagnosis and management of parotitis. Arch Otolaryngol Head Neck Surg. 1992;118:469-471.

2. Fattahi TT, Lyu PE, Van Sickels JE. Management of acute suppurative parotitis. J Oral Maxillofac Surg. 2002;60(4):446-448.

The authors report that they have no conflicts of interest and that no funding was provided for this paper.