Pediatric malignant salivary gland tumors: 60 year follow up.

OBJECTIVE: To evaluate the presentation, treatments and outcomes in pediatric patients with salivary gland malignancies. STUDY DESIGN: Retrospective chart review (1950-2012), Prospective phone interview. METHODS: Patients ≤18 years old with a salivary gland malignancy treated at our institution were identified. Patients were also contacted by phone for a follow up survey. RESULTS: Fifty-six patients were identified. Tumor origin was 88% parotid (n = 49), 5% (n = 3) submandibular and 7% (n = 4) minor salivary glands. Time from onset of symptoms to diagnosis was over one year (mean = 14.4 years). Fifteen out of 52 patients with major gland malignancy had a locoregional recurrence and local recurrences were almost all after initial enucleation. Two of these patients died of disease (overall disease specific survival = 96%). Three out of 4 patients with minor gland malignancy had a local recurrence and two patients with high grade pathology developed metastases and died of their disease (overall survival = 50%). On long term follow up survey in 13 patients (25%), 100% reported normal facial movement and 54% described symptoms of Frey's syndrome, which is higher than other reported series in children. Recurrence was noted up to 45 years after initial treatment. CONCLUSIONS: The majority of malignant pediatric salivary gland tumors are low grade and have excellent survival, especially if found at an early stage. Minor salivary gland malignancies, particularly high grade, have a worse prognosis. Long term mild Frey's syndrome can be expected in approximately half of patients. We advocate a need for long term follow up and increased awareness among providers to diagnose these patients earlier.

Level IIB lymph node metastasis in oropharyngeal squamous cell carcinoma.

OBJECTIVES/HYPOTHESIS: To determine the incidence of level IIB lymph node metastasis in patients with oropharyngeal squamous cell carcinoma (OPSCC) and to evaluate the necessity of level IIB dissection for elective and therapeutic neck dissections. STUDY DESIGN: Retrospective cohort study. METHODS: Patients with OPSCC (N = 348) were surgically managed at our institution from 2004 through 2010. Neck dissection specimens were reviewed by a pathologist, and level IIB metastases were analyzed with respect to clinical and pathologic data. RESULTS: Level IIB lymph node metastases were present in 2.5% and 25% of elective and therapeutic neck dissections, respectively. Level IIA metastasis, clinical tumor stage, clinical nodal stage, extracapsular spread, and primary tumor location in the tonsil were significantly associated with level IIB metastasis. CONCLUSIONS: This study uniquely demonstrated a statistically significant association between clinical tumor stage and tonsil subsite with level IIB metastasis in OPSCC. Considering the predicted incidence of nodal metastasis, we conclude that level IIB neck dissection can be omitted in early stage (T1 or T2) clinically node negative (cN0) OPSCC. In patients with a cN0 neck and advanced OPSCC (T3 or T4), primary tumor in the tonsil, or ipsilateral clinically node positive (cN(+) ) and contralateral cN0 neck, level IIB dissection should be considered. Level IIB dissection should be performed routinely in patients with cN(+) OPSCC.

Level IIB lymph node metastasis in laryngeal and hypopharyngeal squamous cell carcinoma: single-institution case series and review of the literature.

OBJECTIVES/HYPOTHESIS: To determine the incidence of level IIB lymph node metastasis in patients with laryngeal or hypopharyngeal squamous cell carcinoma and to evaluate the need for elective and therapeutic neck dissection of level IIB. STUDY DESIGN: Retrospective cohort study and review of the literature. METHODS: Patients with laryngeal or hypopharyngeal squamous cell carcinoma (N = 65) were primarily treated with surgery at Mayo Clinic (Rochester, Minnesota) from 2004 through 2010. Neck dissection specimens were analyzed by a pathologist, and metastases to level IIB were reported. In addition, 18 previously published studies, totaling 1,114 neck dissections, were reviewed. RESULTS: Level IIB lymph node metastases were present in 4% and 17% of elective and therapeutic neck dissections, respectively. Ipsilateral IIB metastasis was more common than contralateral IIB metastasis in elective and therapeutic neck dissection specimens. Level IIB lymph node metastasis was not significantly associated with level IIA nodal metastasis, level III nodal metastasis, clinical primary tumor stage, clinical nodal stage, or pathologic confirmation of extracapsular spread in either laryngeal or hypopharyngeal squamous cell carcinoma. CONCLUSIONS: The rate of occult IIB metastasis in laryngeal and hypopharyngeal squamous cell carcinoma is exceedingly low. In a clinically node-negative case, the ipsilateral and contralateral level IIB nodal packet should not be dissected. For clinically node-positive cases, ipsilateral level IIB dissection should be performed; contralateral IIB dissection should be performed only when indicated.

Collision tumor of the facial nerve: a synchronous seventh nerve schwannoma and neurofibroma.

OBJECTIVE: To report a novel case of a collision tumor involving an intraparotid neurofibroma and a mastoid segment facial nerve schwannoma. STUDY DESIGN: Clinical capsule report. SETTING: Tertiary academic referral center. PATIENT: A 29-year-old woman with a 2-year history of an asymptomatic enlarging left infraauricular mass and normal FN function presented to a tertiary care referral center. Computed tomography and magnetic resonance imaging demonstrated a cystic lesion in the deep portion of the parotid gland extending into the stylomastoid foramen. INTERVENTION: The patient underwent superficial parotidectomy, and a cystic parotid mass was found to be intrinsic to the intraparotid facial nerve. A portion of the mass was biopsied, and intraoperative frozen section pathology was consistent with a neurofibroma. A mastoidectomy with FN decompression was then performed until a normal-appearing segment was identified just proximal to the second genu. After biopsy, proximal facial nerve stimulation failed to elicit evoked motor potentials, and en bloc resection was performed. RESULTS: Final pathology demonstrated a schwannoma involving the mastoid segment and a neurofibroma involving the proximal intraparotid facial nerve. CONCLUSION: We report the first case of a facial nerve collision tumor involving an intraparotid neurofibroma and a mastoid segment facial nerve schwannoma. Benign FN sheath tumors of the parotid gland are rare but should be considered in the differential diagnosis of a parotid mass.

The intraparotid facial nerve schwannoma: a diagnostic and management conundrum.

OBJECTIVES: The aims of the study were (1) to review the management strategy and clinical outcomes of all intraparotid facial nerve (FN) schwannomas (PFNSs) treated at a single tertiary academic center from 1975 to 2010 and (2) to summarize all previously reported cases of PFNS in the international literature. STUDY DESIGN: A retrospective cohort study and literature review. METHODS: Fifteen patients were diagnosed and treated at the authors' institution from 1975 to 2010. In addition, 124 published cases were systematically reviewed. RESULTS: The most common presentation of PFNS was a painless parotid mass with normal FN function. Eccentric, loosely attached intraparotid tumors underwent gross total resection with nerve preservation granting satisfactory postoperative FN function, whereas "inseparable" intraparotid tumors were observed in 8 cases with stable long-term size. Lesions that extended into the fallopian canal underwent complete resection with FN sacrifice and nerve grafting in 10 cases, whereas 1 patient received subtotal resection of the intraparotid portion with stereotactic radiotherapy targeting the intratemporal component. CONCLUSIONS: Intraparotid FN schwannomas present similar to other primary salivary gland neoplasms, making an early diagnosis challenging. Intraoperative recognition of gross tumor characteristics and early histologic diagnosis with strategic biopsy are critical. Information including tumor location and extent, preoperative FN function, and the gross relationship between the tumor and the FN may guide the surgeon toward an optimal treatment plan emphasizing long-term neurologic preservation.

Location of bacterial biofilm in the mucus overlying the adenoid by light microscopy.

OBJECTIVE: To determine the location of bacteria and biofilm in adenoid tissue and in mucus overlying the adenoid. DESIGN: Adenoids removed in 1 piece were oriented to the cephalic and caudal ends. Mucus was fixed by the gradual addition of Carnoy fluid. Consecutive histologic sections were stained with periodic acid-Schiff for visualization of the exopolysaccharide matrix, Giemsa for visualization of bacteria and cells, and fluorescent in situ hybridization with a universal probe for visualization of bacteria. SETTING: Department of Otolaryngology-Head and Neck Surgery, University of Virginia. PARTICIPANTS: We obtained adenoids from children 10 years or younger who had chronic adenotonsillitis or obstructive sleep apnea. Twenty-seven adenoids were used to develop the fixation method. We examined histologic sections from 9 of 10 adenoids fixed using the final fixation protocol. One adenoid that was missing the surface epithelium was excluded from further evaluation. MAIN OUTCOME MEASURE: Identification of bacteria by light microscopy. RESULTS: Bacteria in large numbers were present in the mucus overlying the surface of all 9 adenoids; bacteria were not found in the parenchyma of the adenoids below the epithelial surface. Bacterial biofilms were present on 8 of the 9 adenoids. Sessile (attached) biofilm was present on the caudal end of only 1 adenoid. Multiple planktonic (unattached) biofilms were present on 7 adenoids, always in areas not subject to mucus flow. Biofilms were most common on the caudal portions of adenoids. CONCLUSIONS: Bacteria of the adenoid reside in secretions on the surface and in crypts. Biofilms, predominantly planktonic, were present on 8 of 9 adenoids excised because of hypertrophy. Whether biofilms have a role in the causation of adenoid hypertrophy is not known.