Introduction
Ductal stenosis produces symptoms of obstruction once luminal diameter is reduced below 1.6 mm (~30% loss of diameter) when fully dilated. Unlike stones, ductal stenosis is more common in the parotid gland (75% of cases) possibly due to the smaller dilated diameter of Stensen’s duct compared with Wharton’s duct (2.5 mm vs 3.0 mm), and the increased predilection of inflammatory and autoimmune disorders to affect the parotid gland. Overall, complications related to endoscopic treatment of salivary stenosis are similar to those of stones (see Chapter 26 ).
Stenosis-Related Complications
Patients who present with obstructive symptoms with meals but without a visible stone will likely have some degree of duct stenosis. Sialendoscopy for stenosis typically involves visualization of the stenosis, followed by serial dilation with hydrostatic pressure, basket, scope tip, guidewire, and malleable bougies, or balloon ( 
).
Inability to Insert the Scope
Inability to insert the scope is a common issue in the endoscopic management of salivary duct stenosis. The ostium itself, which is the narrowest point of a normal duct, may be a site of ductal scar in up to 20% of cases. Scarring of the ostia is particularly common with Wharton’s duct, since the ostia is not supported by a well-formed papilla and the floor of the mouth is more prone to mechanical trauma. Patients with duct stenosis should be scheduled earlier in the operative day to prevent worsening dehydration associated with NPO status, which reduces salivary flow, making ostial identification more difficult. If the ostium is too small to accommodate dilators, a guidewire and bougie dilation can be attempted ( Fig. 31.1A ). However, the surgeon must be prepared for a “cut-down” dichotomy approach. For Wharton’s duct, a cut-down along the floor of the mouth 5 mm from the ostium will allow identification of the distal duct, which can be opened along its superior surface with an 11 blade to allow the scope to enter the duct. The opening can be converted to a neo-ostium with a formal sialodochoplasty ( Fig. 31.1B ).
Ductal Perforation
Ductal perforation is the most common iatrogenic complication encountered during the endoscopic management of ductal stenosis. Overly deep or aggressive dilation may lead to inadvertent perforation of stiff and brittle ductal scar, which is often present in the distal main duct. Perforation is associated with surgeon experience with complication rates as high as 10% during a surgeon’s first 50 cases, with steady decreases to around 2% long term. Wharton’s duct perforations are more common due to a less well-formed papilla, mobile floor of mouth mucosa, and steep angulation of the scope required by the lower dentition. Perforation will nevertheless occur, even with experienced surgeons. This is largely due to scarring of the ostium and thickening of the duct with chronic glandular inflammation, which results in reduced lumen and ductal elasticity preventing proper dilation with irrigation and scope insertion. In most cases, the surgery can proceed following ductal perforation assuming it is rapidly recognized and ameliorated. Signs of perforation include visualization of fat or cobwebs (connective tissue) upon scope insertion, or swelling in the floor of the mouth or anterior cheek ( 
). When recognized, stop irrigation, slowly withdraw the scope until the ductal lumen is visualized, and pass a guidewire down the natural lumen. The guidewire will allow the scope to redirect into the natural duct, or allow passage of a malleable dilator in order to make the duct the path of least resistance when the scope is re-inserted. The surgery can then proceed without the need of additional intervention. Stenting is not required for small perforations, since re-establishment of salivary flow will maintain the lumen and allow healing of the perforation. Larger perforations, which continue to accumulate irrigant in the soft tissues of the cheek or floor of the mouth even after proper cannulation of the duct, require additional measures of repair. Placement of a stent (e.g. 18-guage angiocath; 6 French neonatal nasogastric tube; or salivary specific stent) for 1 week will allow healing of most large Stensen’s duct perforations and prevent sialocele formation. Larger perforations of Wharton’s duct may require small drainage incisions in the floor of the mouth mucosa at the end of the procedure to allow egress of accumulated irrigant and protect the airway upon extubation. Consideration should be given to performing an open sialodochoplasty proximal to the perforation, to prevent a traumatic ranula.
Glandular Swelling
Glandular swelling is common (15–20%) after sialendoscopy for stenosis but typically resolves within 24–48 h. Prolonged swelling (>5 days) is infrequent (4–5%) and will generally resolve with conservative measures. The swelling can be due to overuse of irrigation and/or local tissue trauma and inflammation. The surgeon should take measures to reduce over-irrigation at the time of sialendoscopy by applying irrigation in pulses that allow visualization while avoiding constant irrigation. Removal of the scope with massage of the gland to express irrigant should be intermittently performed during longer procedures. The use of intraoperative intravenous and postoperative oral steroids may additionally reduce the frequency and severity of glandular swelling.
Persistent Symptoms
Persistent symptoms are more common after sialendoscopy for stenosis than stones. Compared with stones, gland-preserving surgery for stenosis has a higher rate of ongoing symptoms (60% vs 30%) following intervention. Stenosis often results from some other etiology causing chronic inflammation of the ducts and parenchyma, which will persist after the stenosis is treated. Therefore patients should be informed that treatment may lessen obstructive symptoms (swelling with meals) but marginally improve other symptoms (xerostomia; glandular pain) that they may find bothersome.
Persistent symptoms are best managed when the underlying etiology of the stenosis is understood. Some causes of stenosis are evident (e.g. previous radioiodine exposure; ductal trauma); however, most cases are not and require further investigation. If the patient reports a history of dry mouth and dry eyes, SSA and SSB serologies should be considered, although many cases of early onset Sjögren will be seronegative at the time of presentation. If the patient is seronegative but has multigland involvement or evidence of intraglandular lymph nodes on imaging ( Fig. 31.2A ), open biopsy of minor salivary gland tissue is indicated and should be tested for Sjögren’s, sarcoidosis, and IgG4-related disease.
