formation. The superficial parotidectomy was accessed with a standard incision (d). A nerve sparing approach was followed (e) that allowed for delivery of the specimen (f). Histopathology showed chronic sialadenitis with abscess formation (g). The patient displayed resolution of his disease at three years postoperatively (h and i) he displays resolution of his disease.
CHRONIC RECURRENT JUVENILE PAROTITIS
Chronic recurrent juvenile parotitis is the second most common inflammatory disease of the salivary glands in children after mumps (Erkul and Gillespie 2016; Xie et al. 2016). In terms of its frequency, chronic recurrent parotitis in adults is 10 times more common than chronic recurrent parotitis in children (Baurmash 2004). It is characterized by recurrent inflammation of one or both parotid glands, with 73% of cases occurring bilaterally (Shacham et al. 2009). Pain may be present or absent, and the lack of pus is one of the main clinical features associated with this disease. Episodes typically occur every three to four months and each episode lasts four to seven days. Recurrent juvenile parotitis is commonly noted prior to puberty with the peak incidence of chronic recurrent juvenile parotitis being between the ages of three and six years (Shacham et al. 2009). This disease is thought to be self‐limiting with many cases resolving by puberty, although some cases persist in adulthood. It is more common in boys than girls. The disease is made on a clinical basis and is confirmed by ultrasonography or sialography that demonstrates the pathognomonic sialectasis.
Several theories exist regarding the etiology and pathophysiology of chronic recurrent juvenile parotitis. Microbiologic analysis of these cases has identified Streptococcus pneumoniae and Haemophilus influenza in high concentrations in these cases, thereby suggesting that microorganisms are of etiologic significance. An autosomal dominant pattern of inheritance has also been suggested to be involved in some cases. It has also been suggested that congenital abnormalities or strictures of Stensen duct, trauma, foreign bodies with the duct, or a history of viral mumps are etiologic. Regardless of the exact etiology, the pathophysiology of the disease is decreased salivary production with inadequate outflow through the duct that encourages ascending salivary gland infections via the oral cavity (Tucci et al. 2019).
Treatment of Chronic Recurrent Juvenile Parotitis
Treatment recommendations range from conservative measures including antibiotics, massage, and sialagogues and surgical procedures with sialendoscopy. Gland preservation should be the goal of treatment since cases typically resolve (Erkul and Gillespie 2016). Shacham et al. (2009) reported on 70 children with chronic recurrent juvenile parotitis who were treated with sialendoscopy and lavage of the gland with 60 ml of normal saline bilaterally. Dilatation of Stensen ducts was performed in four patients and 100 mg of hydrocortisone was injected into each gland. In 93% of patients treated in this fashion, a single treatment was sufficient to resolve the parotitis and prevent its recurrence. Although encouraging studies demonstrate the benefit of sialendoscopy for chronic recurrent juvenile parotitis, there is a lack of prospective, randomized controlled studies comparing this modality to conservative measures alone. It has been recommended to adopt a watchful waiting approach with conservative measures followed by the performance of sialendoscopy if three episodes occur within a six‐month period or four episodes within one year (Erkul and Gillespie 2016). This approach seems valid since spontaneous regeneration of salivary function has been reported (Galili and Marmary 1985).
Tucci et al. (2019) performed a retrospective study of 110 patients with a diagnosis of chronic recurrent juvenile parotitis who underwent sialography without local anesthesia or sedation. The outcome of the sialography was measured by comparing the number and magnitude of episodes of parotid swelling before and after the procedure. Marked improvement was defined by an outcome that saw no episode of parotid swelling or a reduction of more than 80% of episodes in the first year after the procedure. A nonresponder was defined by no improvement in swelling events or by a reduction of less than 30% events. Partial improvement was defined as decreased but not complete resolution of swelling or with a reduction of episodes from 30 to 80% of episodes in the year after sialography. After performing the sialography, a statistically significant overall recovery of pathology was noted in 98 (89%) of patients with a mean 67.4% reduction in the number of acute episodes of parotid swelling in the year after the procedure. Seventy‐five patients demonstrated a marked improvement in symptoms with a mean reduction of 80.6% of acute attacks. Partial improvement was noted in 23 patients with a mean reduction of the number of episodes of 36.5% in the year after sialography. No remission of swelling was noted in 12 patients. The authors concluded that sialography is an effective therapeutic method for chronic recurrent juvenile parotitis and is associated with low cost and with a low rate of complications.
ACUTE BACTERIAL SUBMANDIBULAR SIALADENITIS
Acute bacterial submandibular sialadenitis (ABSS) is usually associated with physical obstruction of the Wharton duct and therefore presents as swelling associated with the submandibular gland. That said, physical examination of the patient with submandibular swelling may not immediately disclose whether the swelling is related to sialadenitis of the submandibular gland, to neoplastic disease of the submandibular gland, or due to a process extrinsic to the submandibular gland. As such, CT scans become required when the distinction cannot be made entirely on physical findings alone (Figure 3.13a). This notwithstanding, sialolithiasis, the likely cause of obstruction of the duct with resultant submandibular gland swelling, 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 the Wharton duct, but in many cases, complete obstruction to pus and saliva occurs. As in the case of acute bacterial parotitis, imaging studies are also obtained in patients with clinically unequivocal acute bacterial submandibular sialadenitis when signs and symptoms are of a magnitude to justify acquiring CT scans (Figure 3.13b).
Figure 3.13. The CT scan (a) of a 73‐year‐old man with a one‐year history of right submandibular swelling. Physical examination of the neck identified a mass with a differential diagnosis of submandibular gland mass vs. enlarged lymph node in the submandibular region. This CT scan was obtained due to the equivocal nature of the finding on physical examination. Fine needle aspiration biopsy of this mass led to a diagnosis of low‐grade lymphoma. By distinction, a 24‐year‐old woman with right submandibular swelling and pain who underwent a CT scan that identified intense uptake of intravenous contrast of the right submandibular gland indicative of acute bacterial submandibular sialadenitis (b). Fat stranding in the left neck indicative of inflammation is also noted.
Figure 3.14. Algorithm for diagnosis and management of acute bacterial submandibular sialadenitis (ABSS).
Treatment of Acute Bacterial Submandibular Sialadenitis
Treatment of ABSS consists of antibiotic therapy, hydration, avoidance of anti‐sialogogues, and removal of a sialolith, if one is identified (Figure 3.14). Empiric antibiotics used to treat ABSS are similar to those antibiotics used in ABP, including an extended spectrum