Parotitis, Acute and Chronic
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- Parotitis is inflammation of the parotid gland caused by infection, noninfectious systemic illnesses, mechanical obstruction, or medications.
- Can be unilateral or bilateral, acute or chronic
- The parotid gland is the largest of the salivary glands, located lateral to the masseter muscle anteriorly and extending posteriorly over the sternocleidomastoid muscle behind the angle of the mandible.
- It produces exclusively serous secretions, which lack the bacteriostatic properties of mucinous secretions, making the parotid gland more susceptible to infection than other salivary glands.
- The parotid duct, also called the Stensen duct, pierces the buccinator muscle to enter the buccal mucosa just opposite the 2nd maxillary molar.
- The branches of the 7th cranial nerve or “facial nerve” bisect the gland into lobes.
- The parotid gland contains 3 to 24 lymph nodes.
- Viral parotitis is the most common cause of parotitis in children; exact incidence is unknown and has decreased since the advent of the mumps vaccine.
- Acute bacterial parotitis occurs more frequently in elderly patients, neonates (especially preterm infants), and postoperative patients.
- Juvenile recurrent parotitis (JRP) is the second most common inflammatory cause of parotitis in children in the United States; first episode usually occurs between the ages of 3 and 6 years.
- Chronic parotitis mainly affects adults, more often females. The average age of presentation is between 40 and 60 years.
- Chronic bilateral parotid enlargement is a common manifestation of HIV infection; for perinatally HIV-infected children, the average age of onset for parotid enlargement is 5 years.
Etiology and Pathophysiology
- Acute viral parotitis begins as a systemic infection that localizes to the parotid gland, resulting in inflammation and swelling of the gland.
- Mumps, or paramyxovirus, has a predilection for the parotid gland and classically has been linked to parotitis. The virus replicates in the upper respiratory tract and spreads by direct contact or airborne transmission.
- Symptoms usually begin 16 to 18 days after infection.
- Acute bacterial parotitis results from stasis of salivary flow that allows retrograde introduction of bacterial pathogens into the gland, resulting in localized infection.
- Acute parotitis pathogens
- Paramyxovirus (mumps), parainfluenza virus types 1 and 3, influenza A, coxsackievirus, Epstein-Barr virus (EBV)
- Cytomegalovirus (CMV) and adenovirus have been seen in patients with HIV.
- Staphylococcus aureus and anaerobes (oral flora) most commonly
- Streptococcus pneumoniae, viridans streptococci, Escherichia coli, and Haemophilus influenzae (less common)
- Other gram-negative rods, such as Klebsiella, Enterobacter, and Pseudomonas, can be seen in chronically ill or hospitalized patients.
- Bartonella henselae in patients with cat exposure (rare)
- Candida has been isolated in chronically ill or hospitalized patients.
- Actinomyces in patients with a history of trauma or dental caries
- Acute, recurrent parotitis
- JRP may be secondary to chronic inflammation; etiology is unknown, but a genetic predisposition may exist.
- Mechanical: Repeated sialolith formation leads to ductal wall damage, fibrosis, and stricture formation.
- Pneumoparotitis may occur when air is trapped in the ducts of the parotid gland; seen in wind instrument players, glass blowers, scuba divers, and with dental cleaning
- Certain medications and chronic diseases (see “Risk Factors”) predispose to chronic parotitis.
- “Anesthesia mumps”: Possible mechanisms include transient mechanical compression of the Stensen duct by airway devices, loss of muscle tone around the Stensen orifice after neuromuscular relaxants, increased salivary secretion, and increased flexion or rotation of the head during general anesthesia.
- Chronic parotitis in HIV-infected patients can be due to presence of benign lymphoepithelial cysts, follicular hyperplasia of parotid lymph nodes, or diffuse infiltrative lymphocytosis syndrome (DILS), causing infiltration of the parotid gland by CD8 cells.
- Parotitis may be secondary to immune reconstitution after initiation of antiretroviral therapy.
- Pediatric considerations include case reports of acute parotitis as a symptom of Kawasaki disease.
- Acute viral parotitis: lack of mumps, measles, rubella (MMR) vaccination
- Acute bacterial parotitis
- Conditions that predispose to salivary stasis, such as dehydration, debilitation, poor oral hygiene, Sjögren syndrome, cystic fibrosis, bulimia/anorexia, sialolithiasis (stones), ductal stenosis, trauma
- Immunosuppression, HIV, chemotherapy, radiation, malnutrition, alcoholism
- Neonatal parotitis: prematurity, dehydration, low birth weight, ductal obstruction, oral trauma, structural abnormalities, immunosuppression
- JRP: dental malocclusion, congenital duct malformation, genetic factors, immunologic anomalies
- Drug-induced parotitis: medications such as anticholinergics, ACE inhibitors (captopril), antihistamines, tricyclic antidepressants, antipsychotics (phenylbutazone, thioridazine, clozapine), iodine (contrast media), and L-asparaginase
- Chronic parotitis: ductal stenosis, HIV, tuberculosis, Sjögren syndrome, sarcoidosis, uremia, diabetes, gout, and atopy
- MMR vaccination with the first dose between 12 and 15 months and second dose between 4 and 6 years of age; childhood mumps vaccination does not guarantee prevention, due to possibility of waning immunity with time.
- Students in post–high school education without documented mumps immunity should receive 2 doses of the MMR vaccine, 28 days apart.
- Pregnant women should not receive the mumps vaccine, and pregnancy should be avoided for 4 weeks after vaccination.
- Maintain adequate hydration and good dental hygiene; smoking cessation, abstinence from alcohol, and avoidance of chronic purging
Commonly Associated Conditions
Mumps, HIV, Sjögren syndrome, sarcoidosis, sialolithiasis