Introduction
Chronic sialadenitis is the most common benign disease of the major salivary glands and is usually the result of obstruction of salivary flow due to calculi, strictures, or both. Chronic sialadenitis, particularly in the parotid gland, may also be associated with Sjögren syndrome, sarcoidosis, and other forms of granulomatous sialadenitis.
In the pre-antibiotic era, the treatment of chronic and recurrent sialadenitis consisted of adequate hydration, sialagogues, warm compresses, and massage of the affected area. In those cases caused by distal intraductal calculi, the papilla of the duct was incised and the calculus removed, with immediate relief. However, many of these patients later developed recurrent calculi, chronic sialadenitis, ductal stenosis, and fistulous tracts leading to the skin. In these cases, the gland was excised. Even now, when more conservative management fails, surgical excision of the gland is the mainstay of effective treatment.
The introduction of techniques such as sialendoscopy, extracorporeal shockwave lithotripsy, and a combination of sialendoscopy and external surgery ( Fig. 11.1 ) has fundamentally changed the therapeutic approach to chronic sialadenitis and ushered in the era of organ preservation. Zenk et al. described a series of 1154 patients who underwent sialendoscopy in the diagnosis and treatment of sialolithiasis. Using sialendoscopy with extraction of the calculi or in combination with transoral removal of the calculus, only 4% of their patients required removal of the submandibular gland. Likewise, only 4% of their patients eventually required parotidectomy. Marchal described a combined transfacial endoscopic technique to extract large calculi, calculi adherent to the duct, intraparenchymal calculi inaccessible to the endoscope, or following failed attempts at calculi removal with other procedures.
While conservative measures as described above are usually effective in controlling the acute exacerbations of this disease, conventional surgery may become necessary when they fail and the infections become too frequent or too severe for episodic treatment. For instance, we described a series of patients with chronic sialadenitis, some of whose underlying problem was Sjögren disease. The clinical course of these patients was characterized by recurrent parotiditis, which required multiple admissions to the hospital for treatment with intravenous antibiotics. Some of these patients also developed abscesses and one patient developed an abscess with a cutaneous fistula.
My indications for surgery in patients with chronic parotitis are: frequent episodes of parotiditis, recurrent parotiditis requiring hospitalization for intravenous antibiotics and for patients who develop complications such as abscess or fistula formation. The indications for excision of the submandibular gland for chronic sialadenitis are similar.
Total Parotidectomy for Sialadenitis
A modified Blair incision is drawn with a skin marker ( Fig. 11.2A ). A 2-0 silk suture is placed in the earlobe. The skin incision is made with a Colorado tip electrocautery. Once the elevation of the skin flap is complete, hemostasis is obtained and the edges of the skin flap are sewn to the drape (see Chapters 35.1 and 47.1 ).
Some patients will have had spontaneous extrusion of a calculus through the skin surrounding the gland or have a fistulous tract present. An elliptical incision surrounding the tract or calculus is made in the direction of relaxed skin tension lines. The tract is then dissected down through the platysma muscle down to the gland.
Blunt and sharp dissection is carried out along the sternocliedomastoid muscle (SCM) toward the mastoid tip. The greater auricular nerve is identified and transected. The mastoid tip is palpated, completing identification of the first landmark for the facial nerve ( Fig. 11.2B ). The posterior belly of the digastric muscle is skeletonized.
Skin hooks are inserted to retract the preauricular soft tissue. The perichondrium of the external auditory meatus (EAM) is then incised and the end of the scalpel handle is inserted along the anterior aspect of the EAM. The main trunk of the facial nerve is usually found 1–2 cm anterior and inferior to the cartilaginous pointer ( Fig. 11.3 ). Since the nerve exits between the mastoid tip and the boney EAM, I prefer to palpate the boney EAM deep to the pointer for greater accuracy.
The main trunk of the facial nerve is a deep structure which is very constant as it exits the stylomastoid foramen and enters the parotid gland. In children, the nerve, while identified as described above, is more superficial because of the smaller size of the child.
It has been suggested that in cases of chronic parotid sialadenitis, it would be safer to identify a peripheral branch of the nerve and dissect it retrograde to the main trunk, thinking that the area of the main trunk would be obliterated by infection-induced scar tissue. The parotid gland is encased in the parotid-masseteric fascia derived from the superficial layer of the deep cervical fascia, which prevents the infection in the gland from involving the area of the stylomastoid foramen, making dissection in the area very safe and the position of the nerve quite predictable. An exception to this is in the case of a previous superficial parotidectomy during which this area has been dissected.
Even in the midst of infection and fibrosis, by staying in the proper plane, the nerve can be dissected free. The dissection continues anteriorly along the branches of the upper and lower divisions ( Fig. 11.4A ).
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