Case report

A 46-year-old male patient presented with a 5 year history of discomfort and recurrent unilateral parotid swelling precipitated by exercise. He did not report awareness of air entering the salivary duct. Clinical examination was unremarkable with no parotid swelling, no crepitation on palpation and on intraoral examination the parotid duct appeared normal. The patient was aware of a ‘crackling’ sensation when the gland was massaged or palpated. Slightly frothy saliva was expressed on gland massage.

An ultrasound investigation showed multiple hyperechoic spots throughout the gland, representing small focal collections of air ( Fig. 1 ). Sialographic examination was normal although on careful evaluation, tiny filling defects could be noticed in the duct, which would usually have been over looked ( Fig. 2 ). In order to clarify the nature of the filling defects and in an attempt to eliminate them from the parotid duct system a sialendoscopic examination was performed. It demonstrated a thickened parotid duct wall but no salivary debris was observed, which is a common finding with inflammation; streams of small bubbles flowed out of the lesser ducts on peroperative irrigation ( Fig. 3 ).

(a) Multiple air foci are seen on this ultrasound image of the parotid gland (arrowed). (b) Normal parotid gland of another patient.

Left parotid sialogram showing normal duct architecture despite small filling defects (arrowed).

Sialendoscopic images showing air bubbles coming out in clusters (a) and isolated (b).

Discussion

The anatomy of Stensen’s duct normally protects against retrograde influx of air to the parotid gland. The flap of mucosa that houses the parotid papilla, together with the slit-shaped orifice of the duct provide a seal when intraoral pressure increases. In addition, the diameter of the duct orifice is smaller than the duct itself . The duct runs in an oblique course through the buccinator muscle which compresses the duct during contraction . In some individuals, a large increase in intra-oral pressure can overcome normal protective mechanisms and allow air and saliva to enter the parotid duct system. Anatomic abnormalities, including a patulous Stensen’s duct , masseter muscle hypertrophy and buccinator muscle weakness are thought to make individuals more prone to develop pneumoparotitis as well.

The literature contains a number of reports of children and adolescents who have induced parotid inflation to avoid school or gain attention . Non-intentional patients include musicians playing wind instruments, glassblowers , and patients undergoing general anaesthesia cases where positive pressure takes place . Pneumoparotid has also been induced by nose blowing, blowing up balloons, chronic attempts to suppress a cough and rapid decompression whilst scuba diving . Any physical activity associated with forceful exhalation may lead to pneumoparotid.

The clinical picture is complicated by ascending infection of the gland, pneumoparotitis, through contamination from the oral environment . An association has been reported between recurrent pneumoparotitis inflammation and fibrosis of the ducts on sialendoscopy. It seems this may set in motion a cycle of duct dilation, sialectasis and further ductal incompetence .

Pneumoparotid usually presents as a unilateral or bilateral facial swelling over the parotid region. The swelling may be painless or tender and it may be associated with warmth and erythema . There is crepitus on palpation of the gland in 50% of patients and frothy saliva or air bubbles may be noticed coming out from Stensen’s duct with massage of the gland . Swelling may resolve over minutes to hours or it may take days. Extension of air beyond the parotid may produce subcutaneous emphysema of the face, neck, and mediastinum with subsequent pneumothorax .

Extreme cases can be diagnosed mainly from a good history. Large air-filled parotid glands are easily confirmed using CT scanning and/or sialography to show dilatation of the gland and its ducts and entrapment of air. It is the unintentional occurrence with minimal air entry that poses a diagnostic problem.

Ultrasound imaging is cheap and readily available. It is sensitive at picking up small air deposits in the parotid gland and is the investigation of choice when pneumoparotitis is suspected.

In conclusion, pneumoparotitis though considered a rare cause of parotid gland swelling, should be included in the differential diagnosis of recurrent parotid swelling. The use of ultrasound is strongly advised in the diagnosis of superficial swellings in the maxillofacial area in general and for salivary gland problems in particular, it gives a characteristic appearance in pneumoparotitis. It is easy, reliable, non-invasive, cost efficient and provides real time conservative dynamic imaging.