Yamamoto Cranioacupuncture Paris

Figure 2.77. Axial PET scan corresponding to the case illustrated in Figure 2.76. The mass in the right parotid gland (arrow) is hypermetabolic. Also note two foci of intense uptake corresponding to inflammatory changes in the tonsils.

Infected Salivary Gland Scan
Figure 2.78. Axial contrast enhanced CT scan through the parotid glands demonstrating a large mass of heterogenous density and enhancement partially exophytic from the gland. Metastatic squamous cell carcinoma from the scalp was diagnosed.

margins and round or ovoid architecture but without a fatty hilum. Late in the disease, mass can mimic infected or inflammatory nodes with heterogenous borders, enhancement, and necrosis. Late in the disease with extranodal spread the margins blur and are ill-defined. Contrast enhancement is heterogenous. Similar findings are seen on MRI with T1 showing low to intermediate signal pre-contrast and homogenous to heterogenous signal post-contrast depending on intranodal versus extranodal disease. PET with FDG is abnormal in infectious, inflammatory, and neoplastic etiology and is not typically helpful within the parotid, but can aid in localizing the site of the primary lesion as well as other sites of metastases. This can be significant since the incidence of clinically occult neck disease is high in skin cancer metastatic to the parotid gland (Bron, Traynor, and McNeil et al. 2003). Local failure was highest with metastatic squamous cell carcinoma and distant metastases were higher in melanoma (Bron, Traynor, and McNeil et al. 2003).

With either squamous cell carcinoma or melanoma there is also a concern for perineural invasion and spread. Tumors commonly known to have perineural spread in addition to the above include adenoid cystic carcinoma, lymphoma, and schwannoma. The desmoplastic subtype of melanoma has a predilection for neurotropism (Chang, Fischbein, and McCalmont et al. 2004). The peri-neural spread along the facial nerve in the parotid gland and into the skull base at the stylomastoid foramen must be carefully assessed. MRI with contrast is the best means of evaluating the skull base foramina for perineural invasion. Gadolinium enhanced T1 MRI in the coronal plane provides optimal view of the skull base (Chang, Fischbein, and McCalmont et al. 2004). There may also be symptomatic facial nerve involvement with lymph-adenopathy from severe infectious adenopathy or inflammatory diseases such as sarcoidosis.


• Among the choices for imaging of the salivary glands, CT with IV contrast is the most commonly performed procedure. Coronal and sagittal reformatted images provide excellent evaluation of soft tissues in orthogonal planes. The latest generation MDCT scanners provide rapid image acquisition reducing motion artifact and produce exquisite multi-planar reformatted images.

• US has the inherent limitation of being operator dependent and poor at assessing deep lobe of the parotid gland and surveying the neck for lymphadenopathy, as well as time consuming relative to the latest generation MDCT scanners.

• MRI should not be used as a primary imaging modality but reserved for special situations, such as assessment of the skull base for peri-neural spread of tumors. Although MRI provides similar information to CT, it is more susceptible to motion and has longer image acquisition time but has better soft tissue delineation.

• PET/CT can also be utilized for initial diagnosis and staging but excels in localizing recurrent disease in post-surgical or radiation fields. Its limitation is specificity, as inflammatory diseases and some benign lesions can mimic malignant neoplasms, and malignant lesions such as adenoid cystic carcinoma may not demonstrate significantly increased uptake of FDG. A major benefit is its ability to perform combined anatomic and functional evaluation of the head and neck as well as upper and lower torso in the same setting. The serial acquisitions are fused in order to provide a direct anatomic correlate to a focus of radiotracer uptake.

• Newer MRI techniques such as dynamic contrast enhancement, MR sialography, diffusion weighted imaging, MR spectroscopy, and MR microscopy are challenging PET/CT in functional evaluation of salivary gland disease and delineation of benign versus malignant tumors. However, PET/CT with novel tracers may repel this challenge.

• Conventional radionuclide scintigraphic imaging has largely been displaced. However, conventional scintigraphy with 99mTc-pertech-netate can be useful for the evaluation of masses suspected to be Warthin's tumor or oncocytoma, which accumulate the tracer and retain it after washout of the normal gland with acid stimulants. The advent of SPECT/ CT in a similar manner to PET/CT may breathe new life into older scintigraphic exams.

• Radiology continues to provide a very significant contribution to clinicians and surgeons in the diagnosis, staging, and post-therapy follow-up of disease. Because of the complex anatomy of the head and neck, imaging is even more important in evaluation of diseases affecting this region. The anatomic and functional imaging, as well as the direct fusion of data from these methods, has had a beneficial effect on disease treatment and outcome. A close working relationship is important between radiologists and clinicians and surgeons in order to achieve these goals.


Abdel Razek A, Kandeel A, Soliman N et al. 2007. Role of diffusion-weighted echo-planar MR imaging in differentiation of residual or recurrent head and neck tumors and post-treatment changes. Am J Neuroradiol 28:11461152.

Alibek S, Zenk J, Bozzato A, Lell M et al. 2007. The value of dynamic MRI studies in parotid tumors. Academic Radiology 14:701-710.

Ando M, Matsuzaki M, Murofushi, T. 2005. Mucosa-associ-ated lymphoid tissue lymphoma presents as diffuse swelling of the parotid gland. Am J Otolaryngol 26:285-288.

Aribandi M, Wood W, Elston D, Weiss, D. 2006. CT features of plexiform neurofibroma of the submandibular gland. Am J Neuroradiol 27:126-128.

Baba S, Engles J, Huso D et al. 2007. Comparison of uptake of multiple clinical radiotracers into brown adipose tissue under cold-stimulated and nonstimulated conditions. J Nucl Med 48:1715-1723.

Beale T, Madani G. 2006. Anatomy of the salivary glands. Semin Ultrasound CT MRI 27:436-439.

Beaulieu S, Kinaha P, Tseng J et al. 2003. SUV varies with time after injection in 18F-FDG PET of breast cancer: Characterization and method to adjust for time differences. J Nucl Med 44:1044-1050.

Bialek E, Jakubowski W, Zajkowski P et al. 2006. US of the major salivary glands: Anatomy and spatial relationships, pathologic conditions and pitfalls. Radiographics 26:745-763.

Bron L, Traynor S, McNeil E et al. 2003. Primary and meta-static cancer of the parotid: Comparison of clinical behavior in 232 cases. Laryngoscope 113(6):1070-1075.

Bui C, Ching A, Carlos R et al. 2003. Diagnostic accuracy of 2-[fluorine-18]-fluro-2-deoxy-D-glucose positron emission tomography imaging in non-squamous tumors of the head and neck. Invest Radiol 38:593-601.

Burrell S, Van den Abbeele A. 2005. 2-deoxy-2-(F-18)-fluoro-D-glucose positron emission tomography of the head and neck: An atlas of normal uptake and variants. Mol Imaging Biol 7:244-256.

Cermik T, Mavi A, Acikgoz G et al. 2007. FDG PET in detecting primary and recurrent malignant salivary gland tumors. Clin Nucl Med 32(4):286-291.

Chang P, Fischbein N, McCalmont T et al. 2004. Perineural spread of malignant melanoma of the head and neck: Clinical and imaging features. Am J Neuroradiol 25:5-11.

Ching A, Ahuja A, King A et al. 2001. Comparison of the sonographic features of acalculous and calculous submandibular sialadenitis. J Clin Ultrasound 29(6): 332-338.

Cholankeril J, Scioscia P. 1993. Post-traumatic sialoceles and mucoceles of the salivary glands. Clinical Imaging 17(1):41-45.

Cohade C, Mourtzikos K, Wahl R. 2003. USA-Fat: Prevalence is related to ambient outdoor temperature—evaluation with 18F-FDG PET/CT. J Nucl Med 44:12671270.

Cohade C, Osman M, Pannu H, Wahl R. 2003. Uptake in supraclavicular area fat (USA-Fat): Description on 18F-FDG PET/CT. J Nucl Med 44:170-176.

de Ru JA, Van Leeuwen M, Van Benthem P et al. 2007. Do magnetic resonance imaging and ultrasound add anything to the workup of parotid gland tumors? J Oral and Maxillofac Surg 65:945-952.

Delbeke D, Coleman R, Guiberteau M et al. 2006. Procedure guidelines for tumor imaging with 18F-FDG PET/CT. J Nucl Med 47:887-895.

Drumond J. 1995. Tomographic measurements of age changes in the human parotid gland. Gerodontology 12(1):26-30.

Eichhorn K, Iakovos A, Ridder G. 2002. Malignant non-Hodgkin's lymphoma mimicking a benign parotid tumor: Sonographic findings. J Clin Ultrasound 30(1):42-44.

Eida S, Sumi M, Sakihama N et al. 2007. Apparent diffusion coefficient mapping of salivary gland tumors: Prediction of the benignancy and malignancy. Am J Neuroradiol 28:116-121.

Gerstle R, Aylward S, Kromhout-Schiro S, Mukherji S et al. 2000. The role of neural networks in improving the accuracy of MR spectroscopy for the diagnosis of head and neck squamous cell carcinoma. Am J Neuroradiol 21:1133-1138.

Habermann C, Gossrau P, Kooijman H et al. 2007. Monitoring of gustatory stimulation of salivary glands by diffusion weighted MR imaging: Comparison of 1.5 T and 3 T. Am J Neuroradiol 28:1547-1551.

Hadi M, Chen C, Millie W et al. 2007. PET/CT, and 123I-MIBG SPECT: A study of patients being evaluated for pheochromocytoma. J Nucl Med 48:1077-1083.

Hamilton B, Salzman K, Wiggins R, Harnsberger H. 2003. Earring Lesions of the Parotid Tail. Am J Neuroradiol 24:1757-1764.

Henkelman R, Watts J, Kucharczyk W. 1991. High signal intensity in MR images in calcified brain tissue. Radiology 179:199-206.

Holliday R. 1998. Benign lymphoepithelial parotid cysts and hyperplastic cervical adenopathy in AIDS-risk patients: A new CT appearance. Radiology 168:439441.

Hopp E, Mortensen B, Kolbenstvedt A. 2004. Mylohyoid herniation of the sublingual gland diagnosed by magnetic resonance imaging. Dentomaxillofacial Radiology 33:351-353.

Hsu C, Lee C, Wang F, Fang C. 2003. Neurofibroma with increased uptake of F-18-fluoro-2-deoxy-D-glucose interpreted as a metastatic lesion. Annals of Nuclear Medicine 17:609-611.

Huang C, Damrose E, Bhuta S, Abemayor E. 2002. Kuttner tumor (chronic sclerosing sialadenitis). Am J Otolaryngol 23(6):394-397.

Ikeda M, Motoori K, Hanazawa T et al. 2004. Warthin tumor of the parotid gland: Diagnostic value of MR imaging with histopathologic correlation. Am J Neurora-diol 25:1256-1262.

Ikeda K, Tsutomu K, Ha-Kawa S et al. 1996. The usefulness of MR in establishing the diagnosis of parotid pleomor-phic adenoma. Am J Neuroradiol 17:555-559.

Ioannidis J, Lau J. 2003. 18F-FDG PET for the diagnosis and grading of soft-tissue sarcoma: A meta-analysis. J Nucl Med 44:717-724.

Izumi M, Eguchi K, Hideki N et al. 1997. Premature fat deposition in the salivary glands associated with Sjogren's syndrome: MR and CT evidence. Am J Neuroradiol 18(5):951-958.

Jansisyanont P, Blanchaert R, Ord R. 2002. Intraoral minor salivary gland neoplasm: A single institution experience of 80 cases. Int J Oral Maxillofac Surg 31(3):257-261.

Jeong H, Chung M, Son Y et al. 2007. Role of 18-F-FDG PET/CT in management of high-grade salivary gland malignancies. J Nucl Med 48:1237-1244.

Jhanvar Y, Straus D. 2006. The role of PET in lymphoma. J Nucl Med 47:1326-1334.

Kalinowski M, Heverhagen J, Rehberg E, Klose K et al. 2002. Comparative study of MR sialography and digital subtraction sialography for benign salivary gland disorders. Am J Neuroradiol 23:1485-1492.

Kaneda T. 1996. MR of the submandibular gland: Normal and pathologic states. AJR 17:1575-1581.

Keyes J, Harkness B, Greven K et al. 1994. Salivary gland tumors: Pretherapy evaluation with PET. Radiology 192:99-102.

King A, Yeung D, Ahuja A et al. 2005. Salivary gland tumors at in-vivo proton MR spectroscopy. Radiology 237:563-569.

Kinoshita T, Okitsu T. 2004. MR imaging findings of parotid tumors with pathologic diagnostic clues: A pictorial essay. Clinical Imaging 28:93-101.

Kirshenbaum K, Nadimpalli S et al. 1991. Benign lym-phoepithelial parotid tumors in AIDS patients: CT and MR findings in nine cases. Am J Neuroradiol 12:271274.

Koeller K, Alamo L, Adair C, Smirniotopoulos J. 1999. Congenital cystic masses of the neck: Radiologic-patho-logic characteristics. Radiographics 19:121-146.

Kurabayashi T, Ida M, Yasumoto M et al. 2000. MRI of ranulas. Neuroradiology 42(12):917-922.

Lin J, Martel W. 2001. Cross-sectional imaging of peripheral nerve sheath tumors: Characteristic signs on CT, MR imaging and sonography. AJR 176:75-82.

Lowe L, Stokes L, Johnson J et al. 2001. Swelling at the angle of the mandible: Imaging of the pediatric parotid gland and periparotid region. Radiographics 21:12111227.

Macdonald A, Salzman K, Hansberger H. 2003. Giant ranula of the neck: Differentiation from cystic hygroma. Am J Neuroradiol 24:757-761.

MacManus M, Ryan G, Lau E, Wirth A, Hicks R. 2007. Positron emission tomography of stage IV mucosa-asso-ciated lymphoid tissue lymphoma confined to the four major salivary glands. Australian Radiology 51:68-70.

Madani G, Beale T. 2006a. Inflammatory conditions of the salivary glands. Semin Ultrasound CT MRI 27:440451.

Madani G, Beale T. 2006b. Tumors of the salivary glands. Semin Ultrasound CT MRI 27:452-464.

Makariou E, Pikis A, Harley E. 2003. Cystic hygroma of the neck: Associated with a growing venous aneurysm. Am J Neuroradiol 24:2102-2104.

Martin N, Serkers O, Mompoint D, Nahum H. 1992. Facial nerve neuromas: MR imaging-report of four cases. Neu-roradiology 34:62-67.

Martinoli C, Pretolesi F, Del Bono V et al. 1995. Benign lymphoepithelial parotid lesion in HIV-positive patients: Spectrum of findings at gray-scale and Doppler sonogra-phy. AJR 165:975-979.

Miyake H, Matsumoto A, Hori Y et al. 2001. Warthin's tumor of parotid gland on Tc-99m pertechnetate scintig-raphy with lemon juice stimulation: Tc99m uptake, size, and pathologic correlation. Eur Radiol 11(12):2472-2478.

Moonis G, Patel P, Koshkareva Y et al. 2007. Imaging characteristics of recurrent pleomorphic adenoma of the parotid gland. Am J Neuroradiol 28:1532-1536.

Motoori K, Iida Y, Nagai Y et al. 2005. MR imaging of salivary duct carcinoma. Am J Neuroradiol 26:1201-1206.

Motoori K, Yamamoto S, Ueda T et al. 2004. Inter- and intratumoral variability in magnetic resonance imaging of pleomorphic adenoma. J Comput Assist Tomogr 28:233-246.

Nakamoto Y, Tatsumi M, Hammoud D et al. 2005. Normal FDG distribution patterns in the head and neck: PET/CT evaluation. Radiology 234:879-885.

Ollila DF, Leland ER et al. 1999. Parotid region lymphatic mapping and sentinel lymphadenopathy for cutaneous melanoma. Ann of Surg Oncol 6(2):150-154.

Otsuka H, Graham M, Kogame M, Nishitani H. 2005. The impact of FDG-PET in the management of patients with salivary gland malignancy. Annals of Nuclear Medicine 19(8):691-694.

Patel R, Carlos R, Midia M, Mukherji S. 2004. Apparent diffusion coefficient mapping of the normal parotid gland and parotid involvement in patients with systemic connective tissue disorders. Am J Neuroradiol 25:16-20.

Patz E, Lowe V, Hoffman J et al. 1993. Focal pulmonary abnormalities: Evaluation with F-18 fluorodeoxyglucose PET scanning. Radiology 188:487-490.

Roh J, Ryu C, Choi S et al. 2007. Clinical utility of 18F-FDG PET for patients with salivary gland malignancies. J Nucl Med 48:240-246.

Rumboldt Z, Al-Okkaili R, Deveikis J. 2005. Perfusion CT for head and neck tumors: A pilot study. Am J Neuroradiol 26:1178-1185.

Schoder H, Erdi Y, Chao K et al. 2004. Clinical implications of different image reconstruction parameters for interpretation of whole-body PET studies in cancer patients. J Nucl Med 45:559-566.

Shah G. 2002. MR imaging of salivary glands. Mag Reson Clin of N Am 10:631-662.

Shah G, Fischbein N, Patel R, Mukherji S. 2003. Newer MR imaging techniques for head and neck. Magn Reson Clin of N Am 11:449-469.

Sheedy S, Welker K, Delone D, Gilbertson J. 2006. CNS metastases of carcinoma ex pleomorphic adenoma of the parotid gland. Am J Neuroradiol 27:1483-1485.

Shimizu K, Iwai H, Ikeda K et al. 2005. Intraparotid facial nerve schwannoma: A report of five cases and an analysis of MR imaging results. Am J Neuroradiol 26:1328-1330.

Sigal R, Monnet O, De Baere T et al. 1992. Adenoid cystic carcinoma of the head and neck: Evaluation with MR imaging and clinical-pathologic correlation in 27 patients. Radiology 184:95-101.

Sokoloff L. 1961. Local cerebral circulation at rest and during altered cerebral activity induced by anesthesia or visual stimulation. In Kety SS, Elkes J (eds.), The Regional Chemistry, Physiology and Pharmacology of the Nervous System. Oxford: Pergamon Press, pp 107-117.

Sokoloff L. 1986. Cerebral circulation, energy metabolism, and protein synthesis: General characteristics and principles of measurement. In Phelps M, Mazziotta J, Schelbert H (eds.), Positron Emission Tomography and Autoradiography: Principles and Applications for the Brain and Heart. New York: Raven Press, pp. 1-71.

Som P, Brandwein M, Silver A. 1995. Nodal inclusion cysts of the parotid gland and parapharyngeal space: A discussion of lymphoepithelial, AIDS-related parotid and branchial cysts, cystic Warthin's tumors, and cysts in Sjogren's syndrome. Laryngoscope 105(10):1122-1128.

Som P, Curtin H (eds.). 1996. Head and Neck Imaging (3rd ed.). St. Louis: Mosby, pp. 823-914.

Stahl A, Dzewas B, Schwaige W, Weber W. 2002. Excretion of FDG into saliva and its significance for PET imaging. Nuklearmedizin 41:214-216.

Su Y, Liao G, Kang Z, Zou Y. 2006. Application of magnetic resonance virtual endoscopy as a presurgical procedure before sialoendoscopy. Laryngoscope 116:1899-1906.

Sugai S. 2002. Mucosa-associated lymphoid tissue lymphoma in Sjogren's syndrome. AJR 179:485-489.

Suh J, Abenoza P, Galloway H et al. 1992. Peripheral (extracranial) nerve tumors: Correlation of MR imaging and histologic findings. Radiology 183:341-346.

Sumi M, Izumi M, Yonetsu K, Nakamura T. 1999a. Sublingual gland: MR features of normal and diseased states. AJR 172(3):717-722.

Sumi M, Izumi M, Yonetsu K, Nakamura T. 1999b. The MR imaging assessment of submandibular gland sialoadeni-tis secondary to sialolithiasis: Correlation with CT and histopathologic findings. Am J Neuroradiol 20:17371743.

Sumi M, Yamada T, Takagi Y, Nakamura T. 2007. MR imaging of labial glands. Am J Neuroradiol 28:15521556.

Takagi Y, Sumi M, Sumi T et al. 2005a. MR microscopy of the parotid glands in patients with Sjogren's syndrome: Quantitative MR diagnostic criteria. Am J Neuroradiol 26:1207-1214.

Takagi Y, Sumi M, Van Cauteren M, Nakamura T. 2005b. Fast and high resolution MR sialography using a small surface coil. J Magn Reson Imaging 22:29-37.

Takahashi N, Okamoto K, Ohkubo M, Kawana M. 2005. High-resolution magnetic resonance of the extracranial facial nerve and parotid duct: Demonstration of the branches of the intraparotid facial nerve and its relation to parotid tumours by MRI with a surface coil. Clinical Radiology 60:349-354.

Takashima S, Takeuchi N, Morimoto S et al. 1991. MR imaging of Sjogren's syndrome: Correlation with sialography and pathology. J Comput Assist Tomogr 15(3):393-400.

Takashima S, Tomofumi N, Noguchi Y et al. 1992. CT and MR appearances of parotid pseudotumors in Sjo-gren's syndrome. J Comput Assist Tomogr 16(3):376-383.

Tanaka T, Ono K, Habu M et al. 2007. Functional evaluation of the parotid and submandibular glands using dynamic magnetic resonance sialography. Dentomaxillo-facial radiology 36:218-223.

Tatsumi M, Engles J, Ishimori T et al. 2004. Intense 18F-FDG uptake in brown fat can be reduced pharmacologically. J Nucl Med 45:1189-1193.

Thoeny H. 2007. Imaging of salivary gland tumors. Cancer Imaging 7:52-62.

Tonami H, Matoba M, Yokota H et al. 2005. Diagnostic value of FDG PET and salivary gland scintigraphy for parotid tumors. Clin Nucl Med 30(3):170-176.

Tonami H, Munetaka M, Yokota H et al. 2002. Mucosa-associated lymphoid tissue lymphoma in Sjogren's syndrome: Initial and follow-up imaging features. AJR 179:485-489.

Uchida Y, Minoshima S, Kawata T et al. 2005. Diagnostic value of FDG PET and salivary gland scintigraphy for parotid tumors. Clin Nucl Med 30:170176.

Wan Y, Chan S, Chen Y. 2004. Ultrasonography-guided core-needle biopsy of parotid gland masses. Am J Neuroradiol 25:1608-1612.

Wang Y, Chiu E, Rosenberg J, Gambhir S. 2007. Standardized uptake value atlas: Characterization of physiological 2-deoxy-2-[18F]fluoro-D-glucose uptake in normal tissues. Mol Imaging Biol 9(2):83-90.

Warburg O. 1925. Uber den Stoffwechsel der Carcinom-Zelle. Klinsche Wochenschrift 4:534-536.

White D, Davidson H, Harnsberger H et al. 2001. Accessory salivary tissue in the mylohyoid boutonniere: A clinical and radiologic pseudolesion of the oral cavity. Am J Neuroradiol 22:406-412.

Wong K, Ahuja A, King A et al. 2004. Vascular lesion in the parotid gland in adult patients: Diagnosis with highresolution ultrasound and MRI. British J of Radiol 77:600-606.

Yabuuchi H, Fukuya T, Tajima T et al. 2002. Salivary gland tumors: Diagnostic value of gadolinium enhanced dynamic MR imaging with histopathologic correlation. Radiology 226:345-354.

Yerli H, Aydin E, Coskum M et al. 2007. Dynamic multislice CT of parotid gland. J Comput Assist Tomogr 31(2):309-316.

Chapter 3

Infections of the Salivary Glands


Introduction General Considerations Bacterial Salivary Gland Infections Acute Bacterial Parotitis (ABP) Variants of ABP and Their Etiology Diagnosis of ABP Treatment of ABP Chronic (Recurrent or Refractory) Bacterial Parotitis

Treatment of Chronic Bacterial Parotitis Chronic Recurrent Juvenile Parotitis Bartonella henselae (Cat Scratch Disease) Acute Bacterial Submandibular Sialadenitis (ABSS)

Treatment of ABSS Chronic Recurrent Submandibular Sialadenitis Tuberculous Mycobacterial Disease Nontuberculous Mycobacterial Disease Viral Salivary Gland Infections Mumps

Human Immunodeficiency Virus Collagen Sialadenitis Summary References


Most non-neoplastic swellings of the major salivary glands represent acute or chronic infections of these glands. Sialadenitis, a generic term to describe infection of the salivary glands, has a diverse range of signs and symptoms and predisposing factors. Although any of the major and minor salivary glands can become infected, these conditions most commonly occur in the parotid (Figure 3.1) and submandibular (Figure 3.2) glands, with minor salivary gland and sublingual gland infections being very rare. From an etiologic standpoint, these infections may be related to underlying bacterial, viral, fungal, mycobacterial, parasitic, or immunologically mediated infections (Miloro and Goldberg 2002). The most common of these diagnoses include acute bacterial parotitis and acute submandibular sialadenitis (see Table 3.1). A number of risk factors may predispose patients to sialadenitis. The classic risk factor is the hospitalized patient who recently underwent surgery with general anesthesia. Dehydration may exacerbate this condition. In general terms, stasis and decreased salivary flow predispose patients to sialadenitis, although medications and comorbid diagnoses may also contribute to this problem (see Table 3.2).

General Considerations

Evaluation and treatment of the patient with sial-adenitis begins with a thorough history and physical examination. The setting in which the evaluation occurs, for example, a hospital ward vs. an office, may provide information as to the underlying cause of the infection. Many cases of acute bacterial parotitis (ABP) occur in elderly debilitated patients, some of whom are admitted to the hospital, who demonstrate inadequate fluid intake with resultant dehydration. This notwithstanding, many cases of acute bacterial parotitis and sub-mandibular sialadenitis are evaluated initially in an outpatient setting. The formal history taking begins by obtaining the chief complaint. Sialadeni-tis commonly begins as swelling of the salivary gland with pain due to stretching of that gland's innervated capsule. Patients may or may not describe the perception of pus associated with salivary secretions, and the absence of pus may be confirmed on physical examination.

History taking is important so as to disclose the acute or chronic nature of the problem that will a b

Figures 3.1a and 3.1b. A 55-year-old woman with a 1-week history of pain and swelling in the left parotid gland. No pus was present at Stenson's duct. The diagnosis was community acquired acute bacterial parotitis. Conservative measures were instituted, including the use of oral antibiotics, warm compresses to the left face, sialogogues, and digital massage.

Stenson Duct Salivary Gland

Figures 3.1c and 3.1d. Two weeks later, she was asymptomatic, and physical examination revealed resolution of her swelling.

Antibiotics For Sialadenitis

Figure 3.2a. A 45-year-old man with a 6-month history of left submandibular pain and swelling. A clinical diagnosis of chronic submandibular sialadenitis was made.

Sialadenitis Ray

Figure 3.2b. A screening panoramic radiograph was obtained that revealed the presence of a large sialolith in the gland. As such, the obstruction of salivary outflow by the sialolith was responsible for the chronic sialadenitis. This case underscores the importance of obtaining a screening panoramic radiograph in a patient with a clinical diagnosis of sialadenitis, as it permitted expedient diagnosis of sialolithiasis.

Figure 3.2b. A screening panoramic radiograph was obtained that revealed the presence of a large sialolith in the gland. As such, the obstruction of salivary outflow by the sialolith was responsible for the chronic sialadenitis. This case underscores the importance of obtaining a screening panoramic radiograph in a patient with a clinical diagnosis of sialadenitis, as it permitted expedient diagnosis of sialolithiasis.

Bacterial infections Acute bacterial parotitis Chronic bacterial parotitis Chronic recurrent juvenile parotitis Acute suppurative submandibular sialadenitis Chronic recurrent submandibular sialadenitis Acute allergic sialadenitis Viral infections Mumps HIV/AIDS Cytomegalovirus Fungal infections Mycobacterial infections Tuberculosis Atypical mycobacteria Parasitic infections Autoimmune-related infections Systemic lupus erythematosus Sarcoidosis Sjogren's syndrome

Table 3.2. Risk factors associated with salivary gland infections.

Modifiable risk factors Dehydration

Recent surgery and anesthesia Malnutrition Medications Antihistamines Diuretics

Tricyclic antidepressants Phenothiazines Antihypertensives Barbiturates Antisialogogues Anticholinergics Chemotherapeutic agents Sialolithiasis Oral infection Non-modifiable risk factors

Advanced age Relatively non-modifiable risk factors Radiation therapy where cytoprotective agents were not administered Renal failure Hepatic failure Congestive heart failure HIV/AIDS Diabetes mellitus Anorexia nervosa/bulimia Cystic fibrosis Cushing's disease significantly impact on how the sialadenitis is ultimately managed. For the purpose of prognosis and the anticipation as to the possible need for future surgical intervention, an acute sialadenitis is somewhat arbitrarily classified as one where symptoms are less than 1 month in duration, while a chronic sialadenitis is defined as having been present for longer than 1 month. In addition, the history will permit the clinician to assess the risk factors associated with the condition. In so doing, the realization of modifiable vs. relatively non-modifiable vs. non-modifiable risk factors can be determined. For example, dehydration, recent surgery, oral infection, and some medications represent modifiable risk factors predisposing patients to sialadenitis. On the other hand, advanced age is a non-modifiable risk factor, and chronic medical illnesses and radiation therapy constitute relatively non-modifiable risk factors associated with these infections. The distinction between modifiable and relatively non-modifiable risk factors is not intuitive. For example, dehydration is obviously modifiable. The sialadeni-tis associated with diabetes mellitus may abate clinically as evidenced by decreased swelling and pain; however, the underlying medical condition is not reversible. The same is true for HIV/AIDS. While much medical comorbidity can be controlled and palliated, these conditions often are not curable such that patients may be fraught with recurrent sialadenitis at unpredictable time frames following the initial event. As such these and many other risk factors are considered relatively non-modifiable.

Other features of the history, such as the presence or absence of prandial pain, may direct the physical and radiographic examinations to the existence of an obstructive phenomenon. The presence of medical conditions and the use of medications to manage these conditions are very important elements of the history taking of a patient with a chief complaint suggestive of sialadenitis. They may be determined to be of etiologic significance when the physical examination confirms the diagnosis of sialadenitis. Musicians playing wind instruments who present for evaluation of bilateral parotid swelling and pain after a concert may have acute air insufflation of the parotid glands as part of the "trumpet blower's syndrome" (Miloro and Goldberg 2002). Recent dental work, specifically the application of orthodontic brackets, may result in traumatic introduction of bacteria into the ductal system with resultant retrograde sialadenitis. Deep facial lacerations proximal to an imaginary line connecting the lateral canthus of the eye to the oral commissure, and along an imaginary line connecting the tragus to the mid-philtrum of the lip, may violate the integrity of Stenson's duct. While a thorough exploration of these wounds with can-nulation and repair of Stenson's duct is meticulously performed, it is possible for foreign bodies to result in obstruction of salivary flow with resultant parotid swelling. A number of autoimmune diseases with immune complex formation can also be responsible for sialadenitis, and confirmation of their diagnosis should be sought during the history and physical examination.

After the history has been completed, the physical examination should be performed. In the patient with suspected sialadenitis, the examination is focused on the head and neck and begins with the extraoral examination followed by the intraoral examination. In particular, the salivary glands should be assessed in a bimanual fashion for asymmetries, erythema, tenderness to palpation, swellings, and warmth. In so doing, one of the most important aspects of this examination is to rule out the presence of a tumor. A neoplastic process of the parotid gland presents as a discrete mass within the gland, with or without symptoms of pain. An infectious process presents as a diffuse enlargement of the parotid gland that is commonly symptomatic. It is possible for an indurated inflammatory lymph node within the parotid gland to simulate neoplastic disease. The distinction in the character of the parotid gland is important so as to not waste time treating a patient for an infectious process when they have a tumor in the parotid gland, particularly in the event of a malignancy. Evidence of facial trauma, including healing facial lacerations or ecchymoses, should be ascertained. The intraoral examination focuses on the observation of the quality and quantity of spontaneous and stimulated salivary flow. It is important to understand, however, that the anxiety and sym-pathomimetic response associated with the examination is likely to decrease salivary flow. Nonetheless, an advanced case of sialadenitis will often allow the clinician to appreciate the flow of pus from the salivary ducts (Figure 3.3). If pus is not observed, mucous plugs, small stones, or "salivary sludge" may be noted. As part of the examination, it may be appropriate to perform cannulation of the salivary duct with a series of lacrimal probes (Figure 3.4). This maneuver may dislodge obstructive material or diagnose an obstruction. The decision to perform this instrumentation, however, must not be made indiscriminately. This procedure

Unilateral Parotitis
Figure 3.3. Pus expressed from Stenson's duct that reflects an acute bacterial parotitis.

Figure 3.4. Lacrimal probes are utilized to probe the salivary ducts. The four shown in this figure incrementally increase in size. Cannulation of salivary ducts begins with the smallest probe and proceeds sequentially to the largest so as to properly dilate the duct. It is recommended that patients initiate a course of antibiotics prior to probing salivary ducts so as to not exacerbate the sialadenitis by introducing oral bacteria into the gland.

may introduce bacteria into the salivary duct that normally colonize around the ductal orifice, thereby permitting retrograde contamination of the gland. This procedure is probably contraindicated in acute bacterial parotitis. The head and neck examination concludes by palpating the regional lymph nodes, including those in the preauricular and cervical regions.

Radiographs of the salivary glands may be obtained after performing the history and physical examination. Since radiographic analysis of the salivary glands is the subject of chapter 2, they will not be discussed in detail in this chapter. Nonethe less, plain films and specialized imaging studies may be of value in evaluating patients with a clinical diagnosis of sialadenitis. Screening plain radiographs such as a panoramic radiograph and/or an occlusal radiograph is important data to obtain when a history exists that suggests an obstructive phenomenon. The presence of a sialolith on plain films, for example, represents very important information with which to direct therapy. It permits the clinician to identify the etiology of the sialadenitis and to remove the stone at an early time frame. Such expedience may permit the avoidance of chro-nicity such that gland function can be maintained.

Bacterial Salivary Gland Infections


World history indicates that acute bacterial parotitis played a significant role in its chronicles, particularly in the United States. We are told that the first case of ABP occurred in Paris in 1829 in a 71-year-old man where the parotitis progressed to gangrene (McQuone 1999; Miloro and Goldberg 2002). As mumps plays a role in the differential diagnosis of infectious parotitis, Brodie's distinction between acute bacterial parotitis and viral mumps in 1834 represents a major inroad into the understanding of this pathologic process (Brodie 1834; Goldberg and Bevilacqua 1995). Prior to the modern surgical era, ABP was not uncommonly observed, and indeed represented a dreaded complication of major surgery, with a mortality rate as high as 50% (Goldberg and Bevilacqua 1995). Ineffective postoperative intravascular volume repletion with resultant diminished salivary flow and dry mouth were the norm rather than the exception. President James Garfield sustained a gunshot wound to the abdomen in July 1881 and developed chronic peritonitis and ultimately died several months later. The terminal event was described as suppurative parotitis that led to sepsis (Goldberg and Bevilacqua 1995). It has been pointed out that upper and lower aerodiges-tive tract surgeries require patients to be without oral nutritional intake or with limited oral intake postoperatively (McQuone 1999). The reduction of salivary stimulation predisposes these patients to acute bacterial parotitis, with an estimated incidence of 1 in 1,000 postoperative patients (Andrews, Abemayor, and Alessi et al. 1989). Other figures showed 3.68 cases per 10,000 operations in the preantibiotic era compared with 0.173 cases per 10,000 operations in the antibiotic era (Robinson

1955). The prophylactic use of antibiotics has probably contributed to the reduction of cases of acute bacterial parotitis. In addition, intraoperative and postoperative intravenous hydration became well accepted in the 1930s, particularly during World War II, therefore also contributing to the reduction in the incidence of ABP. In 1958 Petersdorf reported 7 cases of staphylococcal parotitis, and the 1960s ushered in several reports of ABP as a disease making a comeback (Goldberg and Bevilacqua 1995; Petersdorf, Forsyth, and Bernanke 1958). Of Petersdorf's 7 cases, 5 of the patients had undergone surgery, and 2 of the patients died in the hospital. Oral and maxillofacial surgeons began to report cases of ABP in the literature in the 1960s (Goldberg and Harrigan 1965; Guralnick, Donoff, and Galdabini 1968).

The parotid gland's relative propensity for infection results from physiologic and anatomic factors. Parotid saliva differs from that of the sub-mandibular and sublingual glands. Parotid saliva is predominantly serous compared to the mucinous saliva from the submandibular and sublingual glands. Mucoid saliva contains lysosomes and IgA antibodies that protect against bacterial infection. Mucins also contain sialic acid, which agglutinates bacteria, thereby preventing its adherence to host tissues. Glycoproteins found in mucins bind epithelial cells, thereby inhibiting bacterial attachment to the epithelial cells of the salivary duct.

Variants of ABP and Their Etiology

Over the past several decades changes have occurred in the bacterial flora of the oral cavity that directly reflect the identification of organisms in ABP. In part, this change is evident due to the increased incidence of nosocomial and opportunistic infections in patients who are immunocompro-mised as well as those critically ill patients in hospital intensive care units whose mouths became colonized with micro-organisms that were previously only rarely found in the oral cavity. Moreover, improved culturing techniques have permitted the identification of anaerobes that were previously difficult to recover in the microbiology laboratory. Finally, the occasionally indiscriminate use of antibiotics has allowed for the occupation of other organisms in the oral cavity such as Gramnegative enteric organisms. Bacterial Darwinism has also occurred such that iatrogenically and genetically altered staphylococcal organisms have developed penicillin resistance.

Acute bacterial parotitis has two well-defined presentations, community acquired and hospital acquired variants. Numerous factors predispose the parotid gland to sialadenitis. Retrograde infection is recognized as the major cause of ABP. As a result of acute illness, sepsis, trauma, or surgery, depleted intravascular volume may result in diminished salivary flow that in turn diminishes the normal flushing action of saliva as it passes through Stenson's duct. Patients with salivary secretions of modest flow rates show bacteria at the duct papillae and in cannulated ducts, while patients with salivary secretions of high rates show bacteria at the duct papillae but not within the duct (Katz, Fisher, and Levine 1990). In a healthy state, fibronectin exists in high concentrations within parotid saliva, which promotes the adherence of Streptococcus species and S. aureus around the ductal orifice of Stenson's duct (Katz, Fisher, and Levine 1990). Low levels of fibronectin as occur in the unhealthy host are known to promote the adherence of Pseudomonas and E. coli. This observation explains the clinical situation whereby colonization as a result of dehydration leads to a Gram-positive sialadenitis in ABP compared to the development of Gram-negative sialadenitis of the parotid gland in immunocompro-mised patients (Miloro and Goldberg 2002). Depending on the health of the host, therefore, specific colonized bacteria are able to infect the parotid gland in a retrograde fashion. Hospital acquired ABP still shows cultures of Staphylococcus aureus in over 50% of cases (Goldberg and Bevilacqua 1995). Methicillin resistant Staphylococcus aureus should be ruled out in this population of inpatients. Critically ill and immunocompromised in-patients may also show Pseudomonas, Klebsiella, Escherichia coli, Proteus, Eikenella corrodens, Haemophilus influenzae, Prevotella, and Fusobacte-rium species. Postoperative parotitis has been reported from 1 to 15 weeks following surgery, but most commonly occurs within 2 weeks after surgery (McQuone 1999). The peak incidence of this disease seems to be between postoperative days 5 and 7.

Community acquired ABP is diagnosed five times more commonly than hospital acquired ABP and is diagnosed in emergency departments, offices, and outpatient clinics. This variant of ABP is most commonly associated with staphylococcal and streptococcal species. As community acquired methicillin resistant Staphylococcus aureus becomes more common in society, this organism will become more prevalent in community acquired

ABP. Etiologic factors in community acquired ABP include medications that decrease salivary flow, trauma to Stenson's duct, cheek biting, toothbrush trauma, trumpet blower's syndrome, and medical conditions such as diabetes, malnutrition, and dehydration from acute or chronic gastrointestinal disorders with loss of intravascular volume. Sialo-liths present in Stenson's duct with retrograde infection are less common than in Wharton's duct, but this possibility should also be considered in the patient with community acquired ABP.

Diagnosis of ABP

Diagnosis of ABP requires a thorough history and physical examination followed by laboratory and radiographic corroboration of the clinical diagnosis. Whether occurring in out-patient or in-patient arenas, a history of use of antisialogogue medications, dehydration, malnutrition, diabetes mellitus, immunosuppression, surgery, or systemic disease supports this diagnosis. A predilection for males exists for ABP, and the average age at presentation is 60 years (Miloro and Goldberg 2002). A systemic disorder will result in both glands being affected, but when one gland is affected, the right gland seems to be involved more commonly than the left gland (Miloro and Goldberg 2002). The declaration of acute requires that the parotitis has been present for one month or shorter.

The classic symptoms include an abrupt history of painful swelling of the parotid region, typically when eating. The physical findings are commonly dramatic, with parotid enlargement, often displacing the ear lobe, and tenderness to palpation. If Stenson's duct is patent, milking the gland may produce pus (Figure 3.3). A comparison of salivary flow should be performed by also examining the contralateral parotid gland as well as the bilateral submandibular glands. The identification of pus should alert the clinician to the need to obtain a sterile culture and sensitivity. Constitutional symptoms may be present, including fever and chills, and temperature elevation may exist as long as the gland is infected. If glandular obstruction is present without infection, temperature elevation may not be present. Laboratory values will show a leukocytosis with a bandemia in the presence of true bacterial infection, with elevated hematocrit, blood urea nitrogen, and urine specific gravity if the patient is dehydrated. Electrolyte determinations should be performed in this patient population, particularly in in-patients and out patients who are malnourished. Probing of Sten-son's duct is considered contraindicated in ABP. The concern is for pushing purulent material proxi-mally in the gland, although an argument exists that probing may relieve duct strictures and mucous plugging.

The radiographic assessment of ABP is discussed in detail in chapter 2. Briefly, plain films are of importance so as to rule out sialoliths, and special imaging studies are indicated to further image the parotid gland. The presence of an intra-parotid abscess on special imaging studies, for example, may direct the clinician to the need for expedient incision and drainage.

Treatment of ABP

The treatment of ABP is a function of the setting in which ABP is diagnosed, as well as the severity of the disease within the parotid gland and the presence of medical comorbidities (Figure 3.5). In the outpatient setting, the presence or absence of pus will assist in directing specific therapy. The presence of pus should result in culture and sensitivity. Early species-specific antibiotic therapy is the sine qua non of treatment of ABP. Empiric antibiotic therapy should be based on a Gram stain of ductal exudates. In general terms, an anti-staphylococcal penicillin or a first-generation cephalosporin is a proper choice. Antibiotics should be changed if cultures and sensitivities show methicillin resistant staphylococcal species, in which case clindamycin is indicated in community acquired ABP. In the absence of pus, empiric antibiotic therapy should be instituted as described above. Antibiotic compliance is often difficult for patients such that once- or twice-daily antibiotics are always preferable. In all patients with community acquired ABP, other general measures should be followed including the stimulation of salivary flow with digital massage, the use of dry heat, and the use of sour ball candies. Sugarless sour ball candies should be recommended for diabetics or those with impaired glucose tolerance. Some elderly and debilitated out-patients may require admission to the hospital, in which case intravenous antibiotic therapy will be instituted and incision and drainage may be required. Alteration of anti-sialogogue medications should be accomplished as soon as possible. In the out-patient setting, these commonly include urinary incontinence medications, loop diuretics, beta blockers, and antihistamines. Glycemic control in diabetics is beneficial in the control of ABP. Finally, effective

Parotid swelling

Diffuse enlargement

Discrete mass

Parotid neoplasm

See chapter 8

Parotid swelling?

Purulent drainage at Stenson's duct?


Elevated temperature?

Hospital acquired ABP Community acquired ABP

Culture and sensitivity Empiric intravenous antibiotics Intravenous hydration Heat to face

Discontinue antisialogogues when appropriate Control medical comorbidity

Culture and sensitivity

Empiric oral antibiotics

Oral hydration

Sour ball candies

Discontinue antisialogogues when appropriate Control medical comorbidity

Remove ductal obstruction


Consider sialoendoscopy


No resolution

Incision and drainage Culture and sensitivity

No resolution ^ Parotidectomy

Figure 3.5. Algorithm for treatment of acute bacterial parotitis.

control of viral load in HIV infected patients is of utmost importance.

Imaging of out-patients with community acquired ABP is based on the severity of the clinical disease, its chronicity, and the clinician's suspicion for intra-parotid abscess. Obtaining routine plain films, such as panoramic and occlusal radiographs, is certainly indicated. The main purpose of obtaining these films is to investigate for the presence of a sialolith. It may be acceptable, however, to defer special imaging studies in these patients until refractory infection develops. Patients with severe symptoms, fever, and concern for abscess formation within the parotid gland should be imaged with CT scans in an expedient fashion. Except in the presence of severe immunosuppres-sion or other medical comorbidity, refractory infections are uncommonly seen in ABP.

The general principles of the management of hospital acquired ABP are identical to those of the community acquired ABP. As previously described, however, the risk factors differ. In these in-patients, rehydration should be performed with caution to avoid cardiac overload. Empiric intravenous antibiotics should be instituted in these patients, and confirmed as to their efficacy with culture and sensitivity of purulent parotid exudates whenever possible. The use of heat to the affected gland is appropriate in this setting, as well. The in-patient should be monitored closely for clinical improvement. Despite the institution of conservative measures, if the patient's course deteriorates within 48-72 hours as evident by increased swelling and pain, or an increase in white blood cell count, an incision and drainage procedure is indicated (Figure 3.6). Such a procedure must be guided by CT scans so as to explore all loculations of pus. A needle aspiration of a parotid abscess is unlikely to represent a definitive drainage procedure, although it will permit the procurement of a sample of pus prior to instituting antibiotic therapy in preparation for incision and drainage.

Parotitis Year Old
Figures 3.6a and 3.6b. A 65-year-old man with a 2-week history of left parotid/neck swelling and pain.
Parotid Gland Abscess

Figure 3.6c. Computerized tomograms revealed an abscess within the left parotid gland.

Salivary Gland Abscess
Figure 3.6d. The patient underwent incision and drainage in the operating room for a diagnosis of community acquired acute bacterial parotitis with abscess formation. Methicillin resistant Staph aureus species were cultured.
Parotid Abscess Incision

Figure 3.9b. Computerized tomograms revealed a mass of the left submandibular gland. The patient was taken to the operating room, where excision of the submandibular gland and mass was performed.

Hen Injury Neck Gland Exposed

Figure 3.9e. The specimen.

Stellate Abscess
Figure 3.9f. Histopathology showed a stellate abscess.

Figures 3.9c and 3.9d. Wide access was afforded (c) and the mass was exposed (d).

m-m r à


S*» 7


* % ir'^ 1

^ i


^fiP ■ ï j » Ï

^Tt ■

i f J.^" 3b


«If ^ ,


> *

> **


ft 4 ii


\ P»

s P ¡f!k

zSfcf j




^ „ A


1*.. & if

^fc . " r

Figure 3.9g. A Steiner stain showed Bartonella (gram negative bacillus).

Sialadenitis PathologyKuttner Tumor


Acute bacterial submandibular sialadenitis is usually associated with physical obstruction of Wharton's duct. Since sialolithiasis, the likely cause of obstruction of the duct, is discussed in chapter 5, it is only briefly mentioned here. Suffice it to say that the submandibular ductal system is prone to stone formation. The common features of ABSS are swelling in the submandibular region associated with prandial pain. ABSS is a community acquired disease that less frequently is associated with dehydration and hospitalization as compared to ABP. Purulence may be expressed from the opening of Wharton's duct, but in many cases complete obstruction to pus and saliva occurs.

Treatment of ABSS

Treatment of ABSS consists of antibiotic therapy, hydration, avoidance of anti-sialogogues, and removal of a sialolith, if one is identified. Empiric antibiotics used to treat ABSS are similar to ABP, including an extended-spectrum penicillin, a firstgeneration cephalosporin, clindamycin, or a mac-rolide. Patients are also encouraged to use sialogogues, such as sour ball candies.


Chronic recurrent submandibular sialadenitis usually follows ABSS and is associated with recurrent sialolithiasis. Chronic recurrent submandibu-lar sialadenitis occurs more commonly than chronic recurrent bacterial parotitis. Initial treatment for chronic recurrent submandibular sialadenitis begins with antibiotic therapy, sialogogues, and hydration. Sialoendoscopic intervention may also be of benefit in the treatment of chronic recurrent submandibu-lar sialadenitis prior to subjecting the patient to sialadenectomy. Ultimately, removal of the sub-mandibular gland is often necessary (Figure 3.10).

Figure 3.10a. A 52-year-old man with a 1-year history of vague discomfort in the left upper neck.

Chronic Sialadenitis Pathology Outlines
Figure 3.10c. His diagnosis was chronic submandibular sialadenitis and he was prepared for left submandibular gland excision.
Antibiotics For Sialadenitis

Figure 3.10b. Screening panoramic radiograph showed no evidence of a sialolith.

Figure 3.10d. The surgery was carried through anatomic planes, including the investing layer of the deep cervical fascia.

Sialadenitis Pathology

Figure 3.10e. The dissection is carried deep to this layer since a cancer surgery is not being performed that would require a dissection superficial to the investing fascia. Exposure of the gland demonstrates a small submandibu-lar gland due to scar contracture.

Scar From Salivary Gland Removal

Figures 3.10g and 3.10h. The specimen (g) is bivalved (h), which allows for the appreciation of scar within the gland.

Sialadenitis Pathology
Figure 3.10f. Inferior retraction of the gland allows for identification and preservation of the lingual nerve.

Figure 3.10i. The resultant tissue bed shows the hypo-glossal nerve, which is routinely preserved in excision of the submandibular gland.

Figure 3.10j. Histopathology shows a sclerosing sialadenitis.
Chronic Sclerosing Sialadenitis

Figure 3.10k. The patient's symptoms were eliminated postoperatively, and he healed uneventfully, as noted at 1 year following the surgery.


The most common head and neck manifestation of mycobacterium tuberculosis is infection of the cervical lymph nodes. Tuberculous infection of the salivary glands is generally seen in older children and adults. The infection is believed to originate in the tonsils or gingiva and most commonly ascends to the parotid gland via its duct (Arrieta and McCaffrey 2005). Secondary infection of the salivary glands occurs by way of the lymphatic or hematogenous spread from the lungs. Clinically, tuberculous salivary gland infection presents in two different forms. The first is an acute inflammatory lesion with diffuse glandular edema that may be confused with an acute sialadenitis or abscess. The chronic lesion occurs as a slow-growing mass that mimics a tumor.


Nontuberculous mycobacterial disease has become an important entity in the pediatric population. It has been estimated that greater than 92% of myco-bacterial cervicofacial infections in children are a result of nontuberculous mycobacteria (Arrieta and McCaffrey 2005). The disease primarily affects children younger than 5 years of age. The specific organisms are M. Kansasii, M. avium-intracellulare, and M. scrofulaceum. The typical clinical presentation is that of a rapidly enlarging and persistent parotid and/or neck mass that has failed to resolve with antibiotic therapy (Figure 3.11). A characteristic violaceous discoloration to the skin develops. The treatment of choice is surgical removal of the involved salivary gland and associated lymph nodes.

Parotitis Antibiotic Treatment

Figure 3.11a. 9-year-old girl with a left parotid swelling with overlying erythema of skin but no signs of acute infection. Reprinted from: J. Cranio-Max.-Fac. Surg volume 16, Mitchell DA, Ord RA, Atypical mycobacterial infection presenting as a parotid mass in a child, 221-223, 1988, Georg Thieme Verlag Stuttgart, New York.

Figure 3.11a. 9-year-old girl with a left parotid swelling with overlying erythema of skin but no signs of acute infection. Reprinted from: J. Cranio-Max.-Fac. Surg volume 16, Mitchell DA, Ord RA, Atypical mycobacterial infection presenting as a parotid mass in a child, 221-223, 1988, Georg Thieme Verlag Stuttgart, New York.

Atypical Mycobacterial LymphadenitisUsg Lump Submandibular

Figure 3.11c. Two months following the parotidectomy, a left submandibular lymph node became enlarged and was treated with medical therapy. Reprinted from: J. Cranio-Max.-Fac. Surg volume 16, Mitchell DA, Ord RA, Atypical mycobacterial infection presenting as a parotid mass in a child, 221-223, 1988, Georg Thieme Verlag Stuttgart, New York.

Figure 3.11b. The patient underwent left superficial parotidectomy and excision of a submandibular lymph node. Histo-pathology showed non-caseating granulomas, and cultures showed mycobacterium avium intracellulare. Reprinted from: J. Cranio-Max.-Fac. Surg volume 16, Mitchell DA, Ord RA, Atypical mycobactevial infection presenting as parvotid mass in a child, 221-223, 1988, Georg Thieme Verlag Stuttgart, New York.

Viral Salivary Gland Infections


Viral mumps is an acute, nonsuppurative communicable disease that often occurs in epidemics during the spring and winter months. The term "mumps" is derived from the Danish "mompen," which refers to mumbling, thereby describing the difficulty with speech because of inflammation and trismus (Arrieta and McCaffrey 2005; McQuone 1999). The nearly routine administration of the measles-mumps-rubella (MMR) vaccination has decreased the incidence of mumps in industrialized nations. Since the introduction of the live attenuated vaccine in the United States in 1967 and its administration as part of the MMR vaccine, the yearly incidence of mumps cases has declined from 76 to 2 cases per 100,000 (Murray, Kobayashi, and Pfaller 1994). Mumps characteristically occurs in the parotid glands. Although the disease is typically seen in children between 6 and 8 years of age, it may occur in adults who have avoided childhood infection as well, and displays an equal sex predilection. The disease is caused most commonly by a paramyxovirus, a ribonucleic acid virus related to the influenza and parainfluenza virus groups. Several other nonparamyxoviruses may cause mumps, including coxsackie A and B viruses, Epstein-Barr virus, influenza and parainfluenza viruses, enteric cytopathic human orphan (ECHO) virus, and human immunodeficiency virus (HIV). Mumps is transmitted by infected saliva and urine. The incubation period between exposure and the development of signs and symptoms is 15-18 days. A prodromal period occurs that lasts 24-48 hours and involves fever, chills, headache, and preauricular tenderness. Following the prodromal period, rapid and painful unilateral or bilateral swelling of the parotid glands occurs. Features that distinguish sialadenitis due to mumps vs. bacteria include a lack of purulent discharge, positive serum titers for mumps, and a relative lymphocytosis in mumps. The diagnosis is made by demonstrating complement-fixing soluble (S) antibodies to the nucleoprotein core of the virus, which are the earliest antibodies to appear. These antibodies peak at 10 day

Diabetes Sustenance

Diabetes Sustenance

Get All The Support And Guidance You Need To Be A Success At Dealing With Diabetes The Healthy Way. This Book Is One Of The Most Valuable Resources In The World When It Comes To Learning How Nutritional Supplements Can Control Sugar Levels.

Get My Free Ebook

Post a comment