14 Salivary gland disease
The parotid gland is the largest of the salivary glands. There is considerable variation in size between individuals but for any individual both sides are similar. Although embryologically the parotid consists only of a single lobe, it is convenient to speak of a superficial lobe (superficial to the plane of the branches of the facial nerve) and a deep lobe (deep to that plane). The superficial lobe of the parotid is limited laterally by the preparotid fascia and overlying fat and skin. The zygomatic arch and temporomandibular joint is superior, the masseter muscle is anterior and posteriorly are the cartilaginous external auditory meatus, the mastoid process and the sternocleidomastoid muscle. The isthmus of the parotid gland is bounded by the ramus of the mandible anteriorly and the posterior belly of the digastric behind. The deep lobe is related to the medial pterygoid anteriorly, the styloid apparatus posteromedially and the internal jugular vein. Its deep surface lies immediately superficial to the tonsillar fossa and neoplasms arising from the deep lobe often present as tonsillar masses. The trunk of the facial nerve arises from the stylomastoid foramen just behind the styloid process. It enters the posterior parotid and becomes rapidly more superficial before dividing into two divisions, the superior larger zygomaticotemporal and the smaller buccocervical division. The facial nerve then further divides into five main branches—temporal, zygomatic, buccal, mandibular and cervical—as it passes forwards in a plane separating the superficial and deep lobes. The main collecting duct arises within the superficial lobe and passes horizontally forwards, parallel to the buccal branch in a direction corresponding to a line joining the tragus to a point midway between the alar and the commissure. The duct crosses the masseter muscle horizontally, then turns at right angles to pierce the buccinator muscle and enters the oral cavity at the parotid papilla opposite the second upper molar.
The submandibular gland consists of two lobes—superficial and deep—which are folded over each other posteriorly around the posterior free border of the mylohyoid muscle. The larger superficial lobe lies within the submandibular triangle covered by deep cervical fascia, platysma, fat and skin. The mandibular branch of the facial nerve loops down below the lower border of the mandible. It usually lies on the deep surface of the fascia but may lie between the fascia and the overlying platysma. The deep lobe of the submandibular gland is ‘suspended’ from the lingual nerve and sublingual ganglion by the parasympathetic secretomotor fibres, which must be carefully divided without damaging the sensory fibres of the lingual nerve when removing the gland. The hypoglossal nerve lies in the bed of the deep lobe. The submandibular duct arises from the anterior pole of the deep lobe and runs forwards in the floor of the mouth, crossing the lingual nerve as it passes medially to innervate the tongue.
The sublingual gland is a complex of major and minor salivary glands, which occupies much of the submucosa of the floor of the mouth extending posteriorly to the second molar region. It lies partly within the sublingual fossa of the mandible above the mylohyoid line. Up to 20 small ducts open directly in the floor of the mouth. Some open directly into the submandibular duct.
When considering the many and various conditions and disorders that can affect the salivary glands, it is useful to classify the various conditions according to the standard ‘surgical sieve’ (see Ch. 2).
Mumps (Fig. 14.1) is the most common cause of acute painful parotid swelling affecting children. It is endemic in urban areas and spreads via airborne droplet infection of infected saliva. The disease starts with a prodromal period of 1 or 2 days, during which the child experiences feverishness, chills, nausea, anorexia and headache. This is typically followed by pain and swelling of one or both parotid glands. The parotid pain can be very severe and is exacerbated by eating or drinking. Symptoms resolve spontaneously after 5–10 days. In a classical case of mumps the diagnosis is based on the history and clinical examination: a history of recent contact with an affected patient and bilateral painful parotid swelling is sufficient. However, the presentation may be atypical or sporadic or have predominantly unilateral or even submandibular involvement. In this situation mumps-specific IgM can be identified in the serum as early as 11 days following original exposure to the virus. This antibody is also detectable in the saliva. One episode of infection confers lifelong immunity.
The treatment of mumps is symptomatic. Regular paracetamol and encouragement to maintain fluid intake is important. Complications such as orchitis, oophoritis, meningoencephalitis, pancreatitis and sensorineural deafness are uncommon in children but are more likely in adults. The incidence of mumps is becoming less common as, increasingly, children are receiving the mumps, measles and rubella vaccine at an early age. However, it is important to bear it in mind as a diagnosis whenever a febrile fretful child presents with salivary gland enlargement.
A number of other viral agents—Coxsackie A and B, parainfluenza 1 and 3, ECHO and lymphocytic choriomeningitis—can all cause identical signs and symptoms. Cytomegalic inclusion disease affects mainly newborn infants and children. It is believed to be an intrauterine infection which becomes manifest after birth.
Acute ascending bacterial sialadenitis affects mostly the parotid glands (Fig. 14.2). Historically, it was described in dehydrated, cachectic patients often following major abdominal surgery when the patient was on a ‘nil by mouth’ regime. The reduced salivary flow and oral sepsis resulted in bacteria colonizing the parotid duct and subsequently involving the parotid parenchyma. With current hospital practice and improved oral hygiene, patients are rarely allowed to become dehydrated and this clinical pattern is uncommon. The typical patient presenting with an acute ascending bacterial parotitis now is an otherwise fit young adult with no obvious predisposing factors.
Clinical presentation is of the onset of tender, red, painful parotid swelling over a few hours. There is associated malaise, pyrexia and often regional lymphadenopathy. Pain is exacerbated on attempting to eat or drink. The parotid swelling may be diffuse but often it is localized to the lower pole of the gland, presumably because the infection tends to localize under the effect of gravity.
If the gland is gently ‘milked’ by massaging the cheek cloudy turbid saliva can be expressed from the parotid duct; this should be cultured. The infecting organism is usually Staphylococcus aureus or Streptococcus viridans. Sialography must never be undertaken during the acute phase of infection as the retrograde injection of infected material into the duct system will result in bacteraemia. Ultrasound imaging shows the characteristic dilatation of the acinae.
If the patient presents at an early stage before abscess formation, the infection can usually be controlled with antibiotics. The clinician should not delay waiting for the results of bacterial culture: in a patient not allergic to penicillin a combination of a broad-spectrum penicillin (ampicillin) and a penicillinase-resistant agent (flucloxacillin) is usually effective. In patients allergic to the penicillins, clindamycin is a good alternative. This antibiotic is actively secreted in saliva. The levels in the saliva exceed those in the circulating serum. If the gland becomes fluctuant, indicating abscess formation, the pus must be drained. Occasionally it is possible to drain the abscess by aspirating the pus through a large-bore hypodermic needle, but usually it is necessary to undertake formal surgical drainage under general anaesthesia.
Care must be taken when making the incision not to damage a branch of the facial nerve. Only the skin should be incised and the operation continued with blunt dissection using sinus forceps. A small drain is inserted for 24 hours. Surprisingly, following removal of the drain, the incision heals uneventfully and a salivary fistula does not occur.
Chronic bacterial sialadenitis is far more common in the submandibular salivary gland and usually occurs secondary to chronic obstruction (see below). Unfortunately the submandibular gland has a poor capacity for recovery following infection and in most cases, following control of any acute symptoms with antibiotics, the gland itself must be removed. The operation is performed in hospital under general anaesthesia. Great care must be taken not to damage the mandibular branch of the facial nerve when making the incision, the lingual nerve when mobilizing the gland and clamping the duct and the hypoglossal nerve when separating the gland from the floor of the submandibular triangle.
Chronic sclerosing sialadenitis is a condition that can affect the submandibular gland after a long period of chronic bacterial infection. Progressive atrophy and fibrosis eventually results in a small hard mass, which may undergo dystrophic calcification. This then presents in the submandibular region as a Kuttner tumour (the word tumour being used in its literal sense as a lump and not as a neoplasm).
Recurrent parotitis of childhood exists as a distinct clinical entity but little is known regarding its aetiology and prognosis. It is characterized by the rapid swelling of usually one parotid gland, accompanied by pain and difficulty in chewing, as well as systemic symptoms such as fever and malaise. Although each episode of parotid swelling is usually unilateral, the opposite side may be involved in subsequent episodes. Each episode of pain and swelling lasts for 3–7 days and is followed by a quiescent period of a few weeks to several months. Occasionally episodes are so frequent that the child loses a considerable amount of schooling. The onset is usually between 3 and 6 years, although it has been reported in infants as young as 4 months. The diagnosis is based on the characteristic history and is confirmed by sialography, which shows a very characteristic punctate sialectasis often likened to a snow storm against a dark night sky (Fig. 14.3).
Traditionally the episodes of parotitis have been treated with antibiotics and symptoms settle within 3–5 days on such a regimen. Occasionally, recurrent episodes are so frequent that prophylactic antibiotics are required for a period of months or years. Symptoms seem to resolve spontaneously at puberty but some of these patients go on to develop chronic bacterial parotitis later in life.
A variety of potential allergens causing acute parotid swelling have been identified. Some foods, drugs (most frequently chloramphenicol and tetracycline), metals such as nickel and pollens have been incriminated.
Following the start of therapeutic irradiation, when the parotid glands are within the radiation field the patient develops an acute parotitis, usually after 24 hours. The glands are swollen and tender, there is a marked rise in salivary amylase and the salivary flow rate is reduced. The reaction is self-limiting and resolves after 2 or 3 days, even though the radiotherapy continues. This reaction is quite distinct from the permanent radiation atrophy that occurs with therapeutic doses above 40 Gy, which develops progressively after the radiation has been completed and results in xerostomia.
Chronic parotitis in children is almost pathognomonic of HIV infection. In adults a sicca syndrome and lymphocytic infiltration of the salivary glands are more usual. The presentation of HIV-associated sialadenitis is very similar to classical Sjögren’s syndrome (see later). Dry mouth, dry eyes and swelling of the salivary glands together with lymphadenopathy suggests the diagnosis. Histologically the condition closely resembles Sjögren’s syndrome and differentiation may be difficult. However, autoantibodies—including antinuclear, rheumatoid factor, SS-A and SS-B—are absent unless the patient coincidentally has a connective tissue disorder. AIDS-associated lymphoma presenting as salivary gland swelling has also been described.
Another presentation of salivary gland disease in HIV-positive patients is multiple parotid cysts causing gross parotid swelling and significant facial disfigurement. On imaging with CT or MRI the parotids have the appearance of a Swiss cheese, with multiple large cystic lesions (Fig. 14.4). The glands are not painful and there is no reduction in salivary flow rate. Surgery may be indicated to improve the appearance.
Whenever the major salivary glands are involved, the same histological changes will be present in the minor glands. Similarly, Sjögren’s syndrome invariably involves the minor glands—and indeed the diagnosis is often confirmed on the basis of a minor salivary gland biopsy.
Stomatitis nicotina is a chronic inflammatory disorder of the minor salivary glands of the palate, seen in heavy smokers. The appearance is of multiple small target lesions in which the central opening of the gland is inflamed and bright red, but the surrounding halo of palatal mucosa is white as a result of hyperkeratosis. The condition does not carry a risk of malignant change and is reversible, if the patient can be persuaded to stop smoking.
Acute necrotizing sialometaplasia is an unusual condition, which was first described in 1973. It occurs only on the hard palate in the molar region in the vault of the palate midway between the midline and the gingival margin. It is seen only in heavy smokers. It has a characteristic appearance, which resembles a carcinoma with central ulceration and raised erythematous margins. The ulcer may be as much as 3 cm in diameter. As it so closely resembles a carcinoma the diagnosis is often made on the basis of surgical biopsy. The lesions are self-healing, but often take 10–12 weeks to resolve. As they are extremely painful it is helpful to construct a removable cover plate for the patient to wear, particularly dur/>