OVERVIEW: What every practitioner needs to know
Are you sure your patient has parotitis? What are the typical findings for this disease?
Parotid disease in children can result from multiple etiologies, including infectious, inflammatory, congenital, or neoplastic processes.
The practitioner should differentiate parotitis, or generalized inflammation of the parotid gland, from discrete parotid masses. The most common causes of parotitis in children include mumps, juvenile recurrent parotitis, and suppurative parotitis. There are many congenital lesions and benign or malignant neoplasms of the parotid which may present similarly to parotitis.
In the evaluation of a child with parotitis, the key elements of the history include onset and duration of symptoms and whether involvement is unilateral or bilateral. Key symptoms and signs of major parotid ailments in children include fever, swelling of the face or neck extending to the angle of the mandible, erythema or induration of the overlying skin, and pain or tenderness with motion or palpation. Children may also experience a foul taste from purulent intraoral discharge.
A thorough physical examination for suspected parotitis includes thorough palpation of both parotid glands. Diffuse swelling of the gland should be distinguished from a discrete mass within the gland. A key component of this examination is use of bimanual palpation, in which the fingers of one hand are placed against the buccal (cheek) mucosa while the other hand massages the gland externally from posterior to anterior. The intraoral portion of the gland should also be visualized while massaging the gland, in order to determine whether saliva or purulent material can be expressed from the parotid duct orifice, located in close proximity to the upper second posterior molar.
Additionally, a complete head and neck examination should be performed. Ear exam can rule out any associated middle or external ear disease that may cause periglandular pain. The oral cavity and oropharynx should be throroughly inspected. The neck should also be carefully palpated for associated lymphadenopathy.
Facial nerve function is not typically affected in infectious or inflammatory parotitis. If facial nerve weakness is apparent, malignant lesions should be considered.
Does your patient have mumps?
Mumps is an infectious viral parotitis caused by a paramyxovirus, an enveloped RNA virus, and is the most common cause of parotitis in children worldwide. The infection most characteristically involves the parotid gland but may also affect the gonads, central nervous system (CNS), and pancreas. The incidence of mumps has declined steadily since the institution of routine vaccination programs in most developed countries, however there have been a number of outbreaks in recent years even in vaccinated populations.
What you should consider in the history of a child with mumps:
Mumps infections are most often seen in the winter and spring seasons and may start with a short prodromal stage of low-grade fever, malaise, anorexia, and headache. The hallmark of mumps is painful parotid swelling. Parotid swelling progresses over 2-3 days and lasts for about one week. Swelling typically begins in one gland but will progress to the contralateral gland after several days in 90% of cases.
Orchitis is rare before puberty but occurs in one-third of post-pubertal males with mumps infection. Orchitis is characterized by sudden onset of swelling, warmth, and tenderness of the affected testicle. This generally occurs within 4 to 8 days of parotitis but may occur up to 6 weeks later. In most cases, only one testicle is affected. Constitutional symptoms include high fevers, vomiting, headaches, and malaise. Symptoms progress over 2-3 days and resolve after one week. Gonadal involvement in females is rare, with oophoritis occurring in only 5% of post-pubertal females. Symptoms of oophoritis include lower abdominal pain, fever, and vomiting.
CNS involvement occurs in a minority of mumps infections. Clinically apparent meningitis is seen in 1-10% of mumps infections, and encephalitis in less than 1%. The onset of CNS symptoms typically begins 5 days after the onset of parotitis. Symptoms of mumps meningitis include high fever, headache, neck stiffness, vomiting, and lethargy. Symptoms typically progress over 48 hours and resolve over a period of a week. Mumps encephalitis is characterized by seizures, altered mental status, or focal neurologic deficits.
Characteristic findings on physical exam of child with parotits caused by mumps: On physical examination, unilateral or bilateral parotid swelling and tenderness is characteristic. In many cases, edema and erythema of the parotid duct orifice may be seen. If secretions are expressed from the duct orifice, they are typically thin and clear.
Does your patient have juvenile recurrent parotitis?
Juvenile recurrent parotitis, also called recurrent parotitis of childhood, is characterized by recurrent swelling and inflammation of one or both parotid glands. In the pediatric population, it is the most common cause of parotitis in the United States and the second most common cause of parotitis worldwide. Symptoms generally resolve spontaneously after puberty, though episodes may rarely persist into adulthood. The disease is characterized by sialectasis, or dilation of the distal salivary ducts, resulting in decreased salivary flow, chronic inflammation, and eventual destruction of glandular parenchyma. Its etiology is unknown but thought to be multifactorial.
What you should be alert for in the history of a child with juvenile recurrent parotitis:
Juvenile recurrent parotitis is characterized by intermittent swelling and pain of one or both glands. Symptoms tend to be unilateral. In cases with bilateral involvement, both glands are usually not affected at the same time or symptoms are more pronounced on one side than the other. Episodes are often accompanied by fever and malaise, and symptoms generally last 2-7 days before resolving spontaneously.
The first episode usually occurs between the ages of 2-6 years. As the hallmark of juvenile recurrent parotitis is recurrence, diagnosis is usually delayed until after several episodes have occurred. The average frequency of episodes is one every 3-4 months, though one recent study of 53 patients reported an average of 8 episodes per year with one patient experiencing 100 episodes per year. The frequency of episodes tends to peak during early childhood and then stabilizes until puberty. After puberty, symptoms tend to lessen or resolve completely, and only 10-20% of cases persist into adulthood.
Juvenile recurrent parotitis is more common in males, although approximately one-third of cases are in females.
In children who present with onset of recurrent parotitis after the age of 5-6 years, Sjogren’s syndrome and other autoimmune disorders should be considered.
Characteristic findings on physical exam in a child with juvenile recurrent parotitis: On physical examination, there is unilateral or bilateral parotid swelling and tenderness. The parotid duct orifice is often widened in juvenile recurrent parotitis, though visualizing this may require the use of magnifying lenses. Cloudy saliva may be expressed from the duct orifice. Yellowish plaques may be seen in the saliva. Purulent discharge is not typically expressed.
Does your patient have suppurative parotitis?
Suppurative parotitis, or bacterial sialadenitis, is a bacterial infection of the parotid gland. Suppurative parotitis is most commonly associated with Staphylococcus aureus. This infection is thought to result from salivary stasis, which most often occurs either in the setting of obstruction or decreased salivary production.
What you should be alert for in the history in a child with suppurative parotitis:
Within the pediatric population, suppurative parotitis is most frequently seen in neonates, particularly in premature infants. However, it may occur at any age. The infection typically involves only one gland and is characterized by sudden onset of parotid swelling and pain. There are often constitutional symptoms including high fever, anorexia, and malaise.
Suppurative parotitis typically occurs in the setting of salivary stasis. Patients may have predisposing conditions resulting in decreased salivary production or flow. Practitioners should look for history of dehydration or malnutrition or for use of medications that suppress salivary flow, such as antihistamines. Salivary stasis may also result from obstructive lesions, such as salivary stones or extrinsic masses.
Characteristic findings on physical exam in a child with suppurative parotitis: On physical examination, there is unilateral parotid swelling with induration, warmth, erythema, and tenderness. The parotid duct orifice may be edematous and erythematous. Purulent material is often expressed from the duct orifice with parotid massage.
The parotid region and neck should be palpated to evaluate for regions of fluctuance indicative of possible progress to parotid abscess or deeper neck abscesses.
What other disease/condition shares some of these symptoms?
Less common causes of diffuse parotid inflammation include human immunodeficiency virus (HIV), granulomatous disease, and autoimmune disorders. Parotitis should be distinguished from discrete parotid masses.
What caused parotitis to develop at this time?
Mumps: With the institution of childhood vaccination programs in the United States in the 1960s through 1980s, the incidence of mumps has decreased by 97%. In the United States, there have been two distinct periods of mumps resurgence from the 1980s through 2000s. These outbreaks have tended to be in high schools and colleges located in rural areas. The peak age of infection during these periods was 10-24 years. However, since the last resurgence in 2006, peak incidence has fallen to 5-9 years of age. These more recent outbreaks are thought to perhaps be due to decreased effectiveness of the two-dose vaccine, widely used since 2005, in combination with conditions of crowding seen in college dormitories.
Juvenile recurrent parotitis: Etiology is currently unknown though likely multifactorial in origin. Current theories include recurrent infection (streptococcal), immune deficiency, allergy, genetic factors, and congenital or anatomic defects. Recurrent parotitis may be associated with Sjogren syndrome, and the older the age of onset of recurrent parotitis, the more likely there is an underlying diagnosis of Sjogren disease or other autoimmune disorder. Juvenile recurrent parotitis has also been associated with hypogammaglobulinemia, IgA deficiency, and IgG3 deficiency. One family has been identified with a form of autosomal dominant recurrent parotitis, though no gene has yet been identified.
Suppurative parotitis: This infection occurs in the setting of salivary stasis. This may result from decreased salivary production, which occurs with dehydration or malnutrition or with medications that suppress salivary flow, such as antihistamines. Salivary stasis may also result from obstructive lesions, such as salivary stones or extrinsic compressive masses. Suppurative sialadenitis most often occurs in neonates, particularly in premature infants.
Other causes of parotitis in children:
Atypical mycobacterial infections are not uncommon in young children, particularly those between the ages of 1 and 5 years. Clinically, these infections tend to involve the preauricular, periparotid, and submandibular regions. The lesions tend to be unilateral and painless with overlying violaceous skin changes, and some lesions may form draining sinus tracts. Lesions often persist for several months but are not typically associated with systemic symptoms. Fine needle aspiration may be helpful for diagnosis and for guiding antibiotic therapy. Children may have an intermediate response to standard tuberculin testing. Parotidectomy or excision of infected lymph nodes may be indicated in some cases.
Parotid tuberculosis is rare, especially in developed countries. Clinically, parotid tuberculosis presents as a slow-growing parotid mass with intermittent episodes of pain. Such infections may form draining fistulas to the oral cavity, face, and ear. Fine needle aspiration is useful for diagnosis and helps to avoid unnecessary surgical intervention. Parotid tuberculosis is treated similarly to pulmonary tuberculosis and requires prolonged courses of multi-drug antibiotic therapy.
HIV-associated salivary gland disease is seen in 1-10% of patients with HIV. It most commonly manifests as parotid gland enlargement secondary to the development of benign lymphoepithelial cysts. Clinically, gland enlargement is most often bilateral, painless, slowly progressive, and is usually accompanied by cervical or generalized lymphadenopathy. Treatment for this condition may include antiretroviral therapy and repeat aspiration of the cysts.
Autoimmune disorders may also involve the parotid gland, with Sjogren syndrome being the most common. Sjogren syndrome is an idiopathic systemic autoimmune disorder affecting the exocrine glands, resulting in dry eyes and dry mouth (xerostomia). This disorder primarily affects women in the fourth to fifth decades of life, but cases in children have been reported. Compared to adults, children with Sjogren are more likely to have recurrent parotitis and less likely to have dry eye symptoms. However, laboratory findings are similar, with elevated erythrocyte sedimentation rate (ESR), positive antinuclear antibodies (ANA), positive autoantibodies Ro and La, and lymphocytic infiltration of exocrine glands noted on histopathologic evaluation.
Parotid masses in children: Congenital lesions that may present as masses in the parotid region include branchial cleft cysts and lymphatic malformations.
Branchial anomalies arise from abnormalities of the branchial apparatus during development. Branchial cysts in the parotid or preauricular region often arise from the first branchial cleft and can be intimately involved with the facial nerve. Branchial lesions are benign but can become repeatedly infected. Infection can result in fever, tenderness, and persistent drainage. Infections can be treated by antibiotics, but definitive treatment involves complete surgical resection with identification of the facial nerve.
Lymphatic malformations (formerly known as “lymphangioma” or “cystic hygroma”) arise from abnormalities in lymphatic morphogenesis and may involve the parotid glands. They typically present as a painless, fluctuant, and soft mass which grows in proportion to the patient’s body growth. Lymphatic malformations may present after expansion secondary to trauma, infection, or hormonal stimulus. Lymphatic malformations involving the parotid can be classified as limited to the gland or involving the gland as part of a more extensive cervicofacial lesion. They may be microcystic, macrocystic, or mixed. Parotid lymphatic malformations may be treated with surgical resection or sclerotherapy depending on the quality of the lesion.
Salivary gland neoplasms are rare in children and can be classified as benign tumors, or low- or high-grade malignancies.
Benign neoplasms can be categorized as vascular or nonvascular. The most common vascular tumor in children is infantile hemangioma, which account for 60% of all pediatric salivary gland neoplasms. These tumors undergo an active growth phase of endothelial proliferation followed by a phase of gradual spontaneous involution over several years. One-third are apparent at birth; the remainder will become apparent over the first few weeks of life. The majority (90%) of lesions will regress spontaneously by the age of 9 years; therefore, many lesions do not require medical treatment. If medical therapy is deemed necessary, corticosteroids are the first line of treatment and are effective in 90% of cases.
The most common benign non-vascular tumor of the salivary glands is pleomorphic adenoma, also called benign mixed tumor. Clinically, these tumors present as hard, painless, slow-growing masses and can appear in all age groups. The facial nerve is rarely involved in benign tumors. Removal is recommended due to possibility of malignant transformation over time. Preferred treatment involves surgical resection of the mass with facial nerve preservation.
A solitary parotid mass in a child is more likely to be malignant than in an adult; 50% of pediatric salivary gland tumors are malignant. Malignant tumors may present with pain, rapid growth, or facial weakness. The most common malignant salivary gland tumor in children is mucoepidermoid carcinoma. Other malignant salivary gland tumors include adenoid cystic carcinoma, adenocarcinoma, and undifferentiated carcinoma. Treatment typically requires wide local excision of the mass. Radiation may be required in some cases, for example if there is facial nerve involvement, residual tumor, perineural invasion, or high-grade histologic findings. Some patients may also require treatment of cervical lymph nodes by radiation, lymph node dissection, or both.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
White blood cell count, as well as inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein, may be elevated in any infectious parotitis.
Mumps: In isolated mumps parotitis, white blood cell count is typically normal; however, it may be elevated in cases of mumps orchitis, meningitis, or pancreatitis. Serum amylase levels are typically elevated in mumps parotitis. If confirmation of the diagnosis is sought, this may be done by detection of either viral nucleic acid or an antibody response. Virus can be detected in saliva or CSF within 1 week of symptom onset; however, the ability to detect virus decreases rapidly after the first week. Mumps virus cannot typically be isolated from blood.
Alternatively, diagnosis can also be confirmed by detection of virus-specific IgM antibodies in serum or CSF IgM. Testing is best performed 7-10 days after symptom onset; earlier testing may yield false-negative results. In patients with negative IgM testing, IgG testing of serum may be considered to confirm a prior seroconversion event such as immunization or previous infection.
Juvenile recurrent parotitis: In children with onset of recurrent parotitis after the age of 5-6 years, consider obtaining an autoantibody panel, including antinuclear antibodies (ANA) and rheumatoid factor (RF), as well as serum immunoglobulins. If ANA is positive, consider testing for anti-Ro and La nuclear antibodies. In Sjogren syndrome, ESR is frequently elevated, and ANA, Ro and La antibodies are positive. Patients with Sjogren also tend to have hypergammaglobulinemia.
Suppurative parotitis: If purulent material is expressed from the parotid duct orifice, this should be collected and sent for aerobic culture to enable identification of microorganisms and to guide antibiotic therapy. Specimens taken from the duct orifice should not be sent for anaerobic culture, as this will yield contamination by oral flora. If needle aspiration or surgical drainage is performed, specimens should be sent for both aerobic and anaerobic culture.
Blood cultures may be sent if clinically indicated.
HIV testing should be obtained if any clinical suspicion exists.
Would imaging studies be helpful? If so, which ones?
In the evaluation of parotitis in children, ultrasonography is the preferred initial imaging modality.
Ultrasonography (US): US is an attractive option in children, as it is inexpensive, non-invasive, and requires no sedation or exposure to radiation. For juvenile recurrent parotitis, US is often diagnostic and may show changes consistent with sialectasis (such as multiple hypoechoic regions). US may be helpful in cases of suppurative parotitis to evaluate for sialoliths or progression to parotid abscess. US is also useful for initial characterization of parotid masses, such as distinguishing between cystic or solid lesions, and is used in obtaining guided fine-needle aspiration biopsies in older children. US is particularly useful for determining the vascularity of lesions and should be considered first-line for suspected hemangioma.
Computed tomography (CT): CT with intravenous contrast is useful in the evaluation of a suspected abscess, as well as in evaluation of parotid masses. CT is performed quickly but offers good resolution of not only the parotid glands, but also of surrounding anatomy, which may be beneficial for surgical planning. However, in children, radiation exposure and the need for intravenous contrast should be taken into consideration before proceeding with CT.
Magnetic resonance imaging (MRI): MRI is useful in the evaluation of suspected lymphatic malformations or salivary gland tumors and avoids ionizing radiation. However, given the length of each study, MR imaging usually requires sedation or anesthesia in younger children.
Sialography: Now used rarely, in this technique, radio-opaque dye is injected into the parotid duct and serial radiographs are obtained. This may be used to identify regions of obstruction or dilation of the ductal system. In juvenile recurrent parotitis, sialography may demonstrate multiple round pools of contrast consistent with retained saliva in dilated minor salivary ducts. Sialography is difficult to perform in children without sedation.
If you are able to confirm that the patient has parotitis, what treatment should be initiated?
Treatment is dependent on which form of parotitis is suspected.
Treatment of mumps
Mumps infections are typically mild and self-limited. Treatment involves supportive care, such as analgesics for pain associated with parotitis. There is no specific anti-viral therapy for the mumps virus.
Long-term sequelae of mumps infections are rare. Referral to an otolaryngologist or audiologist should be made for further evaluation if hearing loss is noted.
Treatment of juvenile recurrent parotitis
Conservative management is generally recommended, given that juvenile recurrent parotitis is typically self-limited and resolves after puberty. Treatment of acute attacks involves analgesics, fluid hydration, chewing gum or sialogogues such as lemon drops or sour candy, warm compresses, and parotid massage. Treatment with beta-lactam antibiotics has been suggested but is controversial, as it is unclear if antibiotics change the natural course of each attack or of the disease itself. Antibiotics are indicated if clinical judgment indicates progression to suppurative parotitis or cellulitis.
Prophylactic antibiotics to prevent recurrence are generally considered of no benefit. Measures such as parotid massage and ensuring adequate hydration may help to decrease the frequency or number of episodes. Treatment of acute episodes with antibiotics is controversial; however, many physicians treat episodes with antibiotics targeting routine streptococcal organisms.
Referral to an otolaryngologist is indicated for children with recurrent episodes of parotitis for consideration of other treatment options. Possible treatments include sialendoscopy, in which the parotid duct is dilated and irrigated with normal saline under endoscopic visualization. For recalcitrant cases, total parotidectomy is curative but carries with it a high morbidity rate and is therefore not recommended.
Treatment of suppurative parotitis
Systemic antibiotics with staphylococcus and streptococcus coverage should be initiated; appropriate empiric choices include amoxicillin/clavulanate, metronidazole and a macrolide, or clindamycin for penicillin-allergic patients or in areas with frequent isolates of methicillin-resistant S. aureus. Oral antibiotics may be adequate in some cases, but parenteral antibiotics are required in more severe cases. Total duration of antibiotic therapy should be 10-14 days. Fluid hydration should be encouraged, and sialogogues (lemon drops or sour candy), warm compresses, and parotid massage should also be started.
Surgical drainage may be indicated if clinical improvement is not observed within 24-48 hours of initiating antibiotics, if suppuration is apparent, or if there is facial nerve involvement. Fluctuance may not be evident on physical examination; ultrasonography or CT may help to identify abscess formation. Referral to an otolaryngologist should be made for further management.
What are the possible outcomes of parotitis?
Mumps: Death due to mumps infection is extremely rare; in the pre-vaccination era, the mortality rate was 0.02% in the United States. Mumps infection can result in aseptic meningitis or encephalitis, though symptoms typically resolve after several weeks and long-term neurologic defects are rare. Sensorineural hearing loss may occur but is usually transient. Permanent unilateral hearing loss caused by mumps infection is estimated to occur in one of 20 000 cases. Mumps orchitis is seen in as many as 25% of post-pubertal males with the infection, though mumps-related infertility is rare and even controversial.
Juvenile recurrent parotitis: After puberty, symptoms tend to lessen or resolve completely, with symptoms persisting into adulthood in 10-20% of patients. In one study of 25 patients, symptoms resolved by puberty in 84% and by 22 years of age in 92% of subjects. Though the disease is characterized by gradual destruction of glandular parenchyma, several studies have reported that the damaged parotid gland regenerates following resolution of the disease.
Suppurative parotitis: If left untreated, the infection may spread systemically, resulting in bacteremia or sepsis. The infection can also extend locally to involve surrounding tissues of the head and neck. If a parotid abscess has formed and is left untreated, it may spread through fascial planes to create abscesses of the deep spaces of the neck or the mediastinum.
What causes this disease and how frequent is it?
Detailed epidemiology of mumps:
In the United States, the incidence of mumps is approximately 0.7 per 100 000 population. Infections occur most frequently in the winter and spring, and peak incidence occurs at 5-9 years of age.
Mumps is caused by a paramyxovirus, an enveloped RNA virus which infects only humans. The virus is moderately to highly contagious. Transmission is primarily through droplet spread, though it may also be spread by direct contact or via contaminated fomites. The virus is contagious from 3 days prior to onset of parotid swelling until the swelling has resolved; patients are most infectious 1-2 days prior to onset of swelling. The incubation period is about 14-24 days.
Mumps outbreaks now occur most frequently in crowded environments, such as colleges.
Detailed epidemiology of juvenile recurrent parotitis:
Incidence is unknown. There is no seasonal variation in episodes. The first episode tends to occur between the ages of 2-6 years, and symptoms typically resolve or lessen after puberty.
The etiology of juvenile recurrent parotitis is unclear, and it is controversial whether there is an infectious component to the disorder. The most commonly isolated microorganism in patients with the disorder is Streptococcus viridans, though this bacterial strain is part of normal oral flora. Other organisms that have been implicated include Haemophilus influenzae and Streptococcus pneumoniae. It has been proposed that oral bacteria ascend the salivary duct, causing chronic inflammation and sialectasis.
There are no exposures known to predispose children to juvenile recurrent parotitis.
Detailed epidemiology of suppurative parotitis:
Suppurative parotitis is very rare in children, though incidence is unknown. There is no seasonal variation. In the pediatric population, suppurative parotitis is most frequently seen in neonates, particularly premature infants.
The pathogen most commonly associated with suppurative parotitis is
Staphylococcus aureus. Infections are thought to arise from retrograde movement of oral bacteria in the setting of salivary stasis.
Salivary stasis is thought to predispose patients to develop suppurative infections of the parotid gland. Salivary stasis may result from decreased salivary production, which may occur in dehydration or with medications that suppress salivary flow. Stasis may also occur with lesions that obstruct the salivary duct, such as salivary stones or extrinsic compressive masses.
How do these pathogens/genes/exposures cause the disease?
Mumps: Mumps is acquired through inoculation and viral replication in respiratory mucosa. Transient viremia and infected mononuclear cells allow for systemic spread to the parotid glands and other organs.
Juvenile recurrent parotitis: The etiology of this disorder is unknown, and evidence for an infectious component is mixed. Implicated organisms include Streptococcus viridans, Haemophilus influenzae, and Streptococcus
pneumoniae. It has been postulated that oral bacteria ascend the parotid duct in a retrograde fashion, resulting in chronic inflammation and sialectasis.
Suppurative parotitis: The most common pathogen associated with suppurative parotitis in both neonates and older children is Staphylococcus aureus. Less commonly associated strains include other Gram-positive cocci (such as Streptococcus viridans, Streptococcus pneumoniae, and Streptococcus pyogenes), Gram-negative bacilli (such as Klebsiella pneumoniae, Escherichia coli, and Moraxella catarrhalis), and anaerobic bacteria (such as Peptostreptococcus species and Bacteroides species). Infections are thought to result from retrograde contamination of the salivary ducts by oral bacteria in the setting of salivary stasis, which allows for bacterial growth.
How can parotitis be prevented?
Prophylactic drugs and vaccines: A live attenuated mumps vaccine was first licensed in the United States in 1967, and the vaccine is currently available in this country in a multivalent formulation. In the United States, the Advisory Committee on Immunization Practices (ACIP) currently recommends a two-dose schedule, with the first dose to be administered between 12-15 months of age and the second between 4-6 years.
Prophylactic antibiotics have been suggested for juvenile recurrent parotitis but are generally considered of no benefit.
Behavioral factors: Maintenance of good dental and oral hygiene may help to reduce risk of both juvenile recurrent parotitis and suppurative parotitis.
Nutritional factors: Adequate hydration may help to increase salivary production and flow, thereby reducing risk of both juvenile recurrent parotitis and suppurative parotitis.
What is the evidence?
Adams, DM, Lucky, AW. “Cervicofacial vascular anomalies”. I. Hemangiomas and other benign vascular tumors. Semin Pediatr Surg. vol. 15. 2006. pp. 124-132. (This is an excellent review of the diagnosis and management of hemangiomas.)
Barskey, AE, Glasser, JW, LeBaron, CW. “Mumps resurgences in the United States: A historical perspective on unexpected elements”. Vaccine. vol. 27. 2009. pp. 6186-6195. (The authors provide a historical context for the mumps outbreak that occurred in the United States in 2006, by providing vaccination rates and other surveillance data from 1922 onward.)
Brook, I. “Acute bacterial suppurative parotitis: Microbiology and management”. J Craniofac Surg. vol. 14. 2003. pp. 37-40. (The author reviews the pathogenesis and treatment of acute suppurative parotitis, with a focus on the specific pathogens associated with the disease.)
Brook, I. “The bacteriology of salivary gland infections”. Oral Maxillofacial Surg Clin N Am. vol. 21. 2009. pp. 269-274. (This article provides a thorough review of the microbiology of salivary gland infections in both adults and children.)
Chitre, VV, Premchandra, DJ. “Recurrent parotitis”. Arch Dis Child. vol. 77. 1997. pp. 359-363. (This review discusses the pathogenesis, diagnosis, and treatment of recurrent parotitis.)
Everberg, G. “Deafness following mumps”. Acta Otolaryngol. vol. 48. 1957. pp. 397-403. (The author presents data regarding the development of hearing loss after mumps infection.)
Fattahi, TT, Lyu, PE, Van Sickels, JE. “Management of acute suppurative parotitis”. J Oral Maxillofac Surg. vol. 60. 2002. pp. 446-448. (This article reviews the diagnosis and management of acute suppurative parotitis. It also presents an algorithm for the management of the condition.)
Galazka, AM, Robertson, SE, Kraigher, A. “Mumps and mumps vaccine: A global review”. Bull World Health Organ. vol. 77. 1999. pp. 3-14. (This excellent review provides an overview of the global burden of mumps infection and the impact of mumps vaccination.)
Galili, D, Marmary, Y. “Spontaneous regeneration of the parotid salivary gland following juvenile recurrent parotitis”. Oral Surg Oral Med Oral Pathol. vol. 60. 1985. pp. 605-607. (This case report provides evidence for regeneration of the salivary gland following the resolution of juvenile recurrent parotitis.)
Geterud, A, Lindvall, AM, Nylen, O. “Follow-up study of recurrent parotitis in children”. Ann Otol Rhinol Laryngol. vol. 97. 1988. pp. 341-6. (In this study, the authors provide evidence that symptoms of recurrent juvenile parotitis resolved by adulthood in most patients, though sialectasis remained evident on sialography.)
Hara, T, Nagata, M, Mizuno, Y, Ura, Y, Matsuo, M, Ueda, K. “Recurrent parotid swelling in children: Clinical features useful for differential diagnosis of Sjogren's syndrome”. Acta Paediatr. vol. 81. 1992. pp. 547-549. (The authors provide evidence that children of age 5 years or older presenting with recurrent parotid swelling should undergo evaluation for underlying autoimmune disease.)
Houghton, K, Malleson, P, Cabral, D, Petty, R, Tucker, L. “Primary Sjogren's syndrome in children and adolescents: Are proposed diagnostic criteria applicable?”. J Rheumatol. vol. 32. 2005. pp. 2225-2232. (The authors argue that adult criteria for the diagnosis of Sjogren's syndrome are not appropriate for use in children. They also provide data that recurrent parotitis should raise suspicion for Sjogren's syndrome.)
Hviid, A, Rubin, S, Muhlemann, K. “Mumps”. Lancet. vol. 371. 2008. pp. 932-944. (This is a thorough review of the pathogenesis, symptomatology, diagnosis, and management of mumps infection. It also discusses the mumps vaccination and its impact in detail.)
Katz, P, Hartl, DM, Guerre, A. “Treatment of juvenile recurrent parotitis”. Otolaryngol Clin N Am. vol. 42. 2009. pp. 1087-1091. (The authors briefly review the use of sialendoscopy in the treatment of recurrent juvenile parotitis. They also present their experience with sialography with iodinated oil in 840 children with the disease.)
Leerdam, CM, Martin, HCO, Isaacs, D. “Recurrent parotitis of childhood”. J Paediatr Child Health. vol. 41. 2005. pp. 631-634. (This study retrospectively reviews the presentation, diagnosis, and management of 53 children with juvenile recurrent parotitis.)
Martinez Del Pero, M, Majumdar, S, Bateman, N, Bull, PD. “Presentation of first branchial cleft anomalies: the Sheffield experience”. J Laryngol Otol. vol. 121. 2006. pp. 455-459. (The authors present their experience with first branchial cleft anomalies, including clinical presentation and surgical findings.)
Mehta, D, Willging, JP. “Pediatric salivary gland lesions”. Semin Pediatr Surg. vol. 15. 2006. pp. 76-84. (This is an excellent review of the diagnosis and management of infectious, benign, and neoplastic lesions of the salivary gland in children.)
Patel, A, Karlis, V. “Diagnosis and management of pediatric salivary gland infections”. Oral Maxillofacial Surg Clin N Am. 2009. pp. 345-352. (This article reviews infections of the salivary glands in the pediatric population, including but not limited to juvenile recurrent parotitis.)
Quenin, S, Plouin-Gaudon, I, Marchal, F, Froehlich, P, Disant, F, Faure, F. “Juvenile recurrent parotitis: Sialendoscopic approach”. Arch Otolaryngol Head Neck Surg. vol. 134. 2008. pp. 715-719. (The authors present results of a small prospective study of 10 patients who underwent sialendoscopy for diagnosis and treatment of juvenile recurrent parotitis. They provide evidence that the approach is safe and effective for both diagnosis and management of the disease.)
Reid, E, Douglas, F, Crow, Y, Hollman, A, Gibson, J. “Autosomal dominant juvenile recurrent parotitis”. J Med Genet. vol. 35. 1998. pp. 417-419. (The authors propose that genetic factors may play a role in juvenile recurrent parotitis; they present a family with several members with juvenile recurrent parotitis inherited in an autosomal dominant pattern.)
Schroeder, JW, Mohyuddin, N, Maddalozzo, J. “Branchial anomalies in the pediatric population”. Otolaryngol-Head Neck Surg. vol. 137. 2007. pp. 289-295. (This is a retrospective review of 67 children who underwent surgical treatment of branchial anomalies.)
Shacham, R, Droma, EB, London, D, Bar, T, Nahlieli, O. “Long-term experience with endoscopic diagnosis and treatment of juvenile recurrent parotitis”. J Oral Maxillofac Surg. vol. 67. 2009. pp. 162-167. (The authors present their experience with sialendoscopy in the diagnosis and treatment of 70 children with juvenile recurrent parotitis.)
Shanti, RM, Aziz, SR. “HIV-associated salivary gland disease”. Oral Maxillofac Surg Clin N Am. vol. 21. 2009. pp. 339-343. (This is a review of the different clinical manifestations of HIV in the salivary gland in adults and children.)
Tunkel, DE. “Atypical mycobacterial adenitis presenting as a parotid abscess”. Am J Otolaryngol. vol. 16. 1995. pp. 428-432. (The author presents a case report and thorough review of atypical mycobacterial infection of the parotid gland.)
Wiegand, S, Zimmermann, AP, Eivazi, B, Sesterhenn, AM, Werner, JA. “Lymphatic malformations involving the parotid gland”. Eur J Pediatr Surg. 2011 Mar 15. (This study retrospectively reviews the clinical presentation, management, and outcomes of 20 patients with lymphatic malformations involving the parotid gland.)
Ongoing controversies regarding etiology, diagnosis, treatment
The etiology of juvenile recurrent parotitis is still unknown, and it is unclear if infection plays a role in its pathogenesis. Therefore, the use of antibiotics for the treatment of acute episodes is controversial, with some authors advocating antibiotics only if there is evidence of progression to cellulitis or suppurative parotitis.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has parotitis? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused parotitis to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has parotitis, what treatment should be initiated?
- What are the possible outcomes of parotitis?
- What causes this disease and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- How can parotitis be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment