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syndrome. Sialography if done under general anaesthesia on
table, anticholinergic drugs should be avoided until sialogram
is over, as drugs will reduce salivary flow making difficulty in
identifying the duct orifice.
Findings: Narrowing, (stricture); grape like cluster appear-
ance (sialectasis); dilatations; communications (Fistulas);
mass lesions.
Note:
• Sialography should never be performed in acute inflammation.
• Only 1 mL of dye is injected, if more dye is injected it causes extravasa-
tion and chemical sialadenitis.
• Sialography is contraindicated in acute suppurative sialadenitis. It is
SRB's Manual of Surgery
not useful in neoplasm.
SALIVARY CALCULUS AND SIALADENITIS
80% submandibular; 80% radio-opaque.
It is commonly calcium phosphate and calcium carbonate
stones.
Calculi are more common in submandibular gland, because
the gland secretion is viscous, contains more calcium and
also, its drainage is nondependent, causing stasis.
Secretion from parotid is serous, contains less calcium and
so stones are not common.
Stone is single in 75% of cases.
Incidence of stone in sublingual gland is 1%.
SALIVARY CALCULI
B
Submandibular gland Parotid gland
x 80% common x 20% incidence (Rare)
x 80% radio-opaque x Radiolucent
x Seen in plain X-ray (intraoral) x Not seen in plain X-ray
x Sialogram is not needed x Identified by sialogram
Calculi are common in submandibular salivary gland, because:
x Viscous nature and mucin content
x Calcium content
x Nondependent drainage
x Stasis
x Hooking of nerve by submandibular duct
Fig. 4.10: Stone in the submandibular salivary gland as seen in X-ray
(Courtesy: Dr Jagdish, Mangaluru).
Presentation
Acute Sialadenitis—Features
Pain, swelling, tenderness is seen in submandibular region
and floor of the mouth.
Dysphagia, trismus, fever.
Double chin appearance due to spreading of oedema down-
wards.
Duct is inflamed and swollen.
Treatment is antibiotics, anti-inflammatory drugs.
Causes for submandibular
sialadenitis
• Bacterial—more common. It
is usually due to obstruction
and stasis
• Trauma over duct causing
oedema/stricture and stasis
• Viral—mumps—rare
(Paramyxovirus)
Types of sialadenitis
• Acute
– Bacterial—occurs
following submandibular
salivary ductal
obstruction (Wharton’s)
or in parotid gland. In
parotid, suppuration can
occur leading into parotid
abscess
– Viral—common in parotid
• Chronic—common after
partial obstruction of
submandibular gland
duct or due to stones in
submandibular gland or
hilum proximal to the level of
crossing of the lingual nerve
over the duct
Fig. 4.9: Submandibular sialadenitis in a young boy
who required excision of gland.
Chronic Sialadenitis—Features
Pain is more during mastication due to stimulation (Salivary
colic which can be induced by meals, lemon juice, etc.).
Salivary colic is pain induced by obstruction to the outflow
of saliva may be ductal stone. During salivation size of the
swelling will decrease again 2 hours after meal/stimulation.
Salivary secretion is more during mastication causing
increase in gland size.
Firm/rubbery tender swelling is palpable bidigitally.
When stone is in the duct, it is palpable in the floor of the
mouth as a tender swelling with features of inflammation in
Fig. 4.11: Stone in the duct of submandibular
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salivary gland (Wharton’s duct).
Fig. 4.12: Excised specimen of submandibular
salivary gland with stone in the gland.
In submandibular salivary gland, often the stones are
mul
ti ple, with chronic inflammation of gland (sialadenitis).
Often acute on chronic sialadenitis can occur.
Kuttner tumour is chronic sclerosing sialadenitis of subman-
dibular salivary gland.
Differential diagnosis: Submandibular lymphadenitis; salivary
neoplasm.
Investigations: Intraoral X-ray (dental occlusion films) to see
radio-opaque stones (80%); FNA
C of the gland to rule out other
pathology; total count and ESR in acute phase; USG will demonstrate stone with posterior acoustic shadow. CT scan head and
neck may be occasionally needed to identify the features of the
diseased submandibular salivary gland.
Treatment of Chronic Sialadenitis
Stones <4 mm are removed using sialendoscopy under local
anaesthesia under US guidance. Small sized Dormia basket
is of helpful to retrieve the stone.
Pneumatic lithotripter is very useful to fragment the larger
stones after advancing into the Wharton’s duct under sialendoscope guidance. It shows high success rate.
If stone is in the Wharton’s duct in the floor of the mouth
anterior to the crossing of the lingual nerve, it is removed
by incising the duct longitudinally. Oral mucosa is incised
adequately; sublingual gland is identified and dissected
off the Wharton’s duct laterally; Wharton’s duct is incised
longitudinally from its deeper plane (not from front to avoid
traumatic ranula formation); stone is removed; duct is sutured
using 5 zero absorbable polyglactin interrupted sutures. This
procedure is done under local anaesthesia.
If stone is in the Wharton’s duct behind the crossing of the
lingual nerve it should be removed using intraoral approach
under general anaesthesia only with careful meticulous
dissection. Success rate even though is good; failure to
retrieve stone(s) needs excision of the submandibular salivary
gland through neck approach.
397
CHAPTER 4 Salivary Glands
Fig. 4.13: X-ray (OPG) showing left sided
submandibular salivary stone.
the duct. Pus exudes through the duct orifice. (Irritation of
the lingual nerve, which is in very close proximity to submandibular salivary duct, causes referred pain to tongue—lingual
colic).
Diagnosismeansndingthecauseofthedisorder,notjustgivingitsname.—Sydney Walker
A
Figs. 4.14A and B: Incision for excision of submandibular salivary
gland. It should be 2–4 cm below the margin of the mandible to avoid
injury to marginal mandibular nerve.
B
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In case of deep seated stones in the duct which are not
palpable or stones in the submandibular salivary gland
requires surgical excision.
TECHNIQUE
B
Indications: Chronic sialadenitis; Submandibular salivary tumours
x Approach is from submandibular region (outside). An incision is
made on the skin in submandibular region, about 5–8 cm length,
parallel to and 2–4 cm below the mandible. Incision is deepened
through the deep fascia until the gland is visualised without raising
the flaps (so as to avoid injury to marginal mandibular nerve,
SRB's Manual of Surgery
branch of facial nerve). Facial artery is ligated twice. Lingual nerve
and hypoglossal nerves are taken care of. Mylohyoid is retracted
so as to remove the deep portion of the gland. Drain is placed
after removal of the gland.
x Facial artery lies in the groove on the deeper aspect of the gland;
often embeds in the gland or runs around the gland with a variable course and so artery has to be ligated twice above anteriorly
and below posteriorly.
x Marginal mandibular nerve is in subplatysmal plane in neck,
so incision should be deepened across the deep fascia without
raising subplatysmal plane to avoid injury to this nerve.
x Mobilisation of the gland—intracapsular in sialadenitis; extraca-
psular in tumours with ligation of anterior facial vein.
x Duct identification and ligation; Wound closure with a suction
drain
Complications of Surgery
Haemorrhage; Infection.
Injury to marginal mandibular nerve, lingual nerve, hypo-
glossal nerve.
Injury to nerve to mylohyoid causing anaesthesia over
submental skin.
Note:
• Stone in parotid duct can be removed by opening the duct longitu-
dinally.
• Stone in the gland or in collecting duct is treated by parotidectomy.
• Radiological demonstration of stone/stones is called as sialolithiasis.
Streptococcus viridans and often others like gram-negative
and anaerobic organisms.
CAUSES OF ACUTE PAROTITIS (DIFFERENTIAL DIAGNOSIS
B
OF SUPPURATIVE PAROTITIS)
x Viral—Mumps, Coxsackie virus A and B, parainfluenza 1 and 3,
Echo and lymphocytic choriomeningitis
x Bacterial—Staphylococcus aureus; HIV infection; Syphilis
x Allergic; Radiotherapy, postoperative period
x Sjögren’s syndrome often causes bilateral parotitis
Features
Pyrexia, malaise, pain and trismus.
Red, tender, warm, well-localised, firm swelling is seen in the
parotid region (brawny induration).
Tender lymph nodes are palpable in the neck.
Features of bacteraemia are present in severe cases.
Pus or cloudy turbid saliva may be expressed from the parotid
duct opening.
Investigations: U/S of the parotid region; Pus collected from
duct orifice is sent for culture and sensitivity; Needle aspiration
from the abscess is done to confirm the formation of pus.
Note:
• In suppurative parotitis patient may develop severe laryngeal or pharyn-
geal oedema and may require steroids, tracheostomy and critical care.
• Sialogram is contraindicated in acute phase, as it will cause retrograde
infection leading into bacteraemia.
Complications of suppurative parotitis and parotid abscess:
Septicaemia; Severe trismus; Rupture into the external auditory canal.
Treatment:
¾
Antibiotics are started depending on culture report.
¾
When it is severely tender and localised, incision and
drainage is done under general anaesthesia.
AREAS WHERE ONE SHOULD NOT WAIT FOR THE
B
ABSCESS TO FORM
x Parotid
x Breast
x Ischiorectal fossa
x Thigh
RULE OF 2 IN SUBMANDIBULAR SALIVARY GLAND
B
x 2 parts divided by mylohyoid muscle
x 2 conditions affect it—tumour and stone
x 2 superficial nerves—cervical and mandibular branch of facial
nerves
x 2 deep nerves—lingual and hypoglossal nerves
x Incision—2–4 cm below the mandible
x Ligate facial artery at 2 places
PAROTID ABSCESS (SUPPURATIVE PAROTITIS)
It is a result of an acute bacterial sialadenitis of the parotid
gland.
It is an ascending bacterial parotitis, due to reduced salivary
flow, dehydration, starvation, sepsis, after major surgery,
radiotherapy for oral malignancies and poor oral hygiene.
Parotid fascia is densely thick and tough and so parotid
abscess does not show any fluctuation until very late stage.
Causative organism are Staphylococcus aureus (commonest),
Skin is incised in front of the tragus vertically and then parotid
sheath (pyogenic membrane) is opened horizontally. Pus is
drained using sinus forceps and sent for C/S. Antibiotics are
continued (Blair’s incision).
A B
Figs. 4.15A and B: (A) Parotid abscess; (B) Blair’s incision used to
drain the parotid abscess.
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Proper hydration, mouth wash using povidone iodine/
potassium permanganate solutions, nutrition. Often
patient with parotid infection needs admission and
treatment.
Diagnosis
¾
Sialography to find out the origin of the fistula whether
from parotid gland or duct or ductules; Fistulogram or
CT fistulogram; Discharge study; MRI.
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CHAPTER 4 Salivary Glands
PAROTID FISTULA
Parotid fistula may arise from parotid gland or duct or duct-
ules. It may open inside the mouth as internal fistula; or open
outside onto the skin as external fistula. Fistula from the duct
has profuse discharge. Fistula from the gland often shows
only minimal discharge.
Incidence of salivary fistula is 0.2–3%.
Types
1. Duct fistula forms after superficial parotidectomy. It is profuse
and often persisting. So duct should be ligated using nonabsorbable suture as far as possible, anteriorly to allow normal
saliva drainage from deep lobe. If common duct is ligated
deep lobe atrophies without causing any fistula.
2. Gland fistula occurs from the raw surface after superficial
parotidectomy. It is mild and symptom subsides in a month
with anticholinergic drugs. Jacobsom tympanic neurectomy
completely stops the secretion from the fistula in this type.
CAUSES
B
x After superficial parotidectomy
x After drainage of parotid abscess, ruptured abscess
x After biopsy
x Trauma
x Recurrence of malignant tumour
Features
Discharging fistula in the parotid region of the face, and
discharge is more during eating.
Tenderness and induration; Trismus.
Treatment
Anticholinergics—hyoscine bromide (probanthine).
Radiotherapy.
Often exploration of fistula is required.
Repair or reinsertion of the duct into the mucosa.
Newman Seabrock’s operation—a probe is passed into the
parotid duct through the opening in the mouth. Another
probe is passed through the fistula. Duct and fistula are
dissected over the probe. After removal of the fistula track
severed duct ends are identified; and ends are trimmed.
Probes are removed. A tantalum wire is passed into the duct
across the severed ends and duct is sutured over it using
4 zero vicryl. Tantalum stent is removed after 3 weeks.
If still persists, auriculotemporal nerve which supplies
secretomotor component of parotid is cut.
If there is stenosis at the orifice of the Stenson’s duct, papil-
lotomy at the orifice may help.
Total conservative parotidectomy is done in failed cases.
REMEMBER ABOUT SALIVARY FISTULA
B
x Commonly from the parotid
x It can be internal draining into the mouth or can be external
draining outside
x It is acquired commonly but rarely can be congenital
x It can be due to surgery, trauma or due to sepsis
x Fistula arising from the gland parenchyma drains through suture
line but usually closes spontaneously. Leakage will be more during
meals. Saliva is confirmed by its high amylase content compared
to seroma/serous fluid
x Fistula due to ductal disruption leaks profusely and invariably
needs surgery to close it
x Submandibular gland fistula commonly closes spontaneously,
rarely if not requires complete removal of the gland
x Anticholinergics, irradiation, denervation of the gland, duct liga-
tion are done to reduce saliva production
x Excision of fistula, repair of the duct, diversion of the duct into
the mouth are other options
x In severe intractable cases, removal of the gland/total conservative
parotidectomy is needed
Fig. 4.16: Parotid fistula with discharging saliva and pus.
RECURRENT CHILDHOOD PAROTITIS
It is a recurrent, rapid enlargement of one or both parotids
with fever and malaise in children of age group between 3 and
6 years without any known aetiology. Recurrent episodes with
a quiescent period in between are typical. Sialogram shows
snowstorm punctate sialectasis. Low dose antibiotics for
long period may be required. Occasionally patient may need
total conservative parotidectomy especially if it occurs late in
adolescent period.
By perseverance the snail reached the ark.—Charles Haddon Spurgeon
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SJÖGREN’S SYNDROME
SIALECTASIS
It is an autoimmune disease causing progressive destruction of
salivary and lacrimal glands, leading to keratoconjunctivitis sicca
(dry eyes), and xerostomia (dry mouth).
Types: 1. Primary. 2. Secondary.
Primary Sjögren’s syndrome (Primary Glandular sicca
syndrome) presents with severe dry mouth and dry eyes;
widespread dysfunction of exocrine glands. It has got high
incidence of developing lymphomas. But there is no association of connective tissue disorders.
Secondary Sjögren’s syndrome presents with dry mouth
SRB's Manual of Surgery
and dry eyes; with association of connective tissue disorders
like—Primary biliary cirrhosis (near 100%), SLE (30%),
Rheumatoid arthritis (RA) (15%). Female to male ratio is
10 : 1.
Features
It is common in middle aged females who present with dry
eyes, dry mouth, enlarged parotids and enlarged lacrimal
glands which are often tender. Superadded infections of the
mouth,
Investigations: Autoantibody estimation—rheumatoid factor,
Candida albicans is common.
antinuclear factor, salivary duct antibody, sialography;
estimation of salivary flow; slit lamp test of eyes; Schirmer
test—to detect lack of lacrimal secretion; FNAC of parotids
and lacrimal glands; 99Technetium pertechnetate scan for
gland function.
Treatment: It is conservative. Artificial tears; artificial saliva;
frequent drinking of water; treat the cause.
Note:
• Mikulicz disease: It is a clinical variant of Sjögren’s syndrome. It is
an autoimmune disorder of salivary and lacrimal glands, resulting
in infiltration of the glands with round cells. It may be due to or
associated with sarcoidosis, Sjögren’s syndrome, leukaemia and
lymphoma.
• Triad of Mikulicz disease: (1) Symmetrical and progressive enlarge-
ment of all salivary glands. (2) Narrowing of palpebral fissures due
to enlargement of the lacrimal glands. (3) Parchment-like dryness of
the mouth.
• Primary extra-glandular sicca syndrome: Dry mouth, dry eyes,
hyperglobulinaemic purpura, vasculitis, Raynaud’s phenomenon or B
cell lymphoma.
• In benign lymphoepithelial lesion, 20% bilateral diffuse parotid
swelling develops; 20% develop lymphoma.
SIALOSIS
It is enlargement of the salivary gland due to fatty infiltration,
as a result of various metabolic causes like diabetes, acromegaly, obesity, liver disease, alcoholism, bulimia, idiopathic,
drug induced (sympathomimetics, carbimazole, thiouracil).
It is diffuse, bilateral, non-inflammatory, non-neoplastic
asymptomatic swelling of the salivary gland mostly of
parotids with fatty infiltration and acinar cell hypertrophy.
Clinical features: Bilateral diffuse enlargement of parotids,
which is smooth, firm, non-tender.
Treatment: The cause is treated.
It is an aseptic dilatation of salivary ductules causing grape-
like (cluster-like) dilatations.
It is a disease of unknown aetiology with destruction of
parenchyma of gland accompanied by stenosis and cyst
formation in the ductules.
It is common in parotids; often bilateral.
Presents as a smooth, soft, fluctuant, nontransillu minating
swelling which increases in size during mastication. It is
tender initially. It lasts for many days with a long symptomfree period of the disease.
Sialogram is diagnostic (grape or cluster-like dilata tions).
Treatment is conservative (nonsurgical).
SALIVARY NEOPLASMS
Aetiology
Genetic—loss of alleles of chromosomes in 12q, 8q, 17q.
Eskimos are more prone for salivary neoplasm.
Infective—mumps, Epstein-Barr virus, chronic sialadenitis
may be the cause; but not proved emphatically. Recurrent
inflammation can cause duct dysplasia and carcinoma.
Radiation—it is more common in survivors of atomic bomb
explosion; mucoepidermoid carcinoma is more in these
patients.
Smoking—adenolymphoma of Warthin’s shows 40% risk
in smokers.
Sex—benign tumours and many malignancies are common
in females; Warthin’s and some malignancies are common
in males.
Environment and diet—Arctic-Eskimos show dietary defi-
ciency of vitamin A and develop salivary tumour. Industrial
agents like nickel, cadmium, hair dyes, silica, preservatives
may increase the risk of salivary tumours.
Classication (WHO)
a. Epithelial (90%):
1.
Adenomas
–
Pleomorphic adenoma.
–
Monomorphic adenomas.
»
Adenolymphoma (Warthin’s tumour).
»
Oncocytoma (oxyphil adenoma) seen in elderly;
seen in parotid gland.
»
Basal cell adenoma—it is a rare benign tumour.
2. Carcinomas
–
Mucoepidermoid carcinoma—most common malignancy.
–
Acinic cell carcinoma—1%.
–
Adenoid cystic carcinoma—very aggressive—10%;
common minor salivary glands.
–
Adenocarcinoma.
–
Squamous cell carcinoma—2%.
–
Carcinoma in ex pleomorphic adenoma.
–
Undifferentiated carcinoma.
Note:
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Carcinoma can be:
• Low grade (acinic cell; adenoid cystic; low grade mucoepidermoid) or
• High grade (adenocarcinoma; squamous cell carcinoma; high grade
mucoepidermoid) mesenchymal.
Fig. 4.17: Parotid enlargement in a boy of 11-year-old.
b. Nonepithelial:
Haemangioma—commonly seen in infants, usually in
parotids. Spontaneous regression is common. Most common
benign salivary gland tumour in paediatric age group.
Lymphangioma.
Neurofibromas and neurilemmomas.
c.
Malignant lymphomas—NHL type:
Common in parotids.
Common with HIV, Sjögren’s syndrome (44 times more
chances than normal people).
d. Secondary tumours from head and neck region; bronchus
and skin.
be diffuse/focal/capsulated/unencapsulated. It may
be associated with Mikulicz’s disease or Sjögren’s
syndrome.
¾
Malignant—it is rare tumour occurs in parotid and
submandibular glands (ESKIMOMA).
Incidence
Eighty per cent salivary neoplasms are in the paro tids of
which 80% are benign; 80% of these are pleomorphic
adenomas; 80% occur in superficial lobe.
Fifteen per cent of salivary tumours are in the submandibular
salivary gland, of which 50% are benign. 95% of these are
pleomorphic adenomas.
Ten per cent of salivary neoplasms are in the minor salivary
glands—palate, lips, cheeks, etc. Of these only 10% are benign.
Note:
• Parotid tumours are common but only 20% are malignant.
• Submandibular tumours are uncommon but 50% of them are malignant.
• Minor salivary gland tumours are rare and 90% of them are malignant.
• Sublingual salivary tumours are very rare but almost all sublingual
salivary tumours are malignant.
• Incidence of malignancy in salivary glands is inversely related to size of
the gland; in parotid it is 15%; in submandibular it is 50%; in sublingual
it is 85%.
PLEOMORPHIC ADENOMA
(Mixed Salivary Tumour)
Commonest of the salivary gland tumour in adult.
It is 80% common.
More common in parotids (80%). 10% in submandibular
salivary gland; 0.5% in sublingual salivary gland.
It is mesenchymal, myoepithelial and duct reserve cell origin.
Grossly it contains cartilages, cystic spaces, solid tissues.
Microscopically it is biphasic in nature with epithelial and
stromal components. Benign tumours will usually not show
necrosis.
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CHAPTER 4 Salivary Glands
Figs. 4.18A and B: Neoplasm of parotid gland (Malignant).
e. Lymphoepithelial tumours:
¾
Benign—it is 5% of all benign salivary tumours
(Godwin’s tumour). It is common in females; can be
bilateral. Benign lymphoepithelial lesion (BLEL) is
of unknown etiology characterized by replacement
of salivary parenchyma with lymphoid tissue. It may
Selecting wisely generally follows experience of selecting unwisely; from this experience comes sound judgement usually
HISTOLOGICALLY IT SHOWS:
B
x Epithelial cells
x Myoepithelial cells
Even though it is capsulated, tumour may come out as
x Mucoid material with myxo-
matous changes
x Cartilages/pseudocartilages
pseudopods and may extend beyond the main limit of the
BA
tumour tissue.
When disease occurs in parotid, commonly it involves super-
ficial lobe or superficial and deep lobe together.
But sometimes only deep lobe is involved and then it presents
as swelling in the lateral wall of the pharynx, soft palate and
posterior pillar of the fauces. There may not be any visible
swelling in the preauricular region. It is called as ‘dumb-
bell tumour’. This tumour is in relation to styloid process,
mandible, stylohyoid, styloglossus, stylopharyngeus muscles.
based on bad judgement.
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SRB's Manual of Surgery
Features
CLINICAL FEATURES OF PAROTID TUMOUR
B
x Swelling, pain, ulceration, dysphagia (if deep lobe is involved)
x Raised ear lobule
x Cannot be moved above the zygomatic bone—curtain sign
x Deviation of uvula and pharyngeal wall towards midline in case
of deep lobe tumour
x Facial nerve, masseter, skin, lymph node and bone involvement
eventually occurs in case of malignancy
Common in females (3:1).
Occurs in any age group. But common in 4th and 5th decade
Usually unilateral.
Present as a single painless, smooth, firm lobulated, mobile
swelling in front of the parotid with positive curtain sign (As
the deep fascia is attached above to the zygomatic bone, it
acts as a curtain, not allowing the parotid swelling to move
above that level. Any swelling superficial to the deep fascia
will move above the zygomatic bone).
Obliteration of retromandibular groove is common.
The ear lobule is raised.
When deep lobe is involved, swelling is commonly located
in the lateral wall of pharynx, posterior pillar and over the
soft palate—10%. Deep lobe tumour passes through Patey’s
stylomandibular tunnel pushing tonsils, pharynx, soft palate
often without any visible swelling or only small swelling
when only deep lobe tumour is present; it also presents as
dysphagia. Bidigital palpation of parotid is significant in such
occasion with one finger inside mouth.
Facial nerve is not involved.
Fig. 4.20: Deep lobe tumour of parotid is examined per orally.
Long-standing pleomorphic adenoma may turn into carcinoma
(carcinoma in ex pleomorphic adenoma). Its features are:
x Recent increase in size
x Pain and nodularity
x Involvement of skin, ulceration
x Involvement of masseter
x Involvement of facial nerve—lower facial nerve palsy—(Difficulty
in closing eyelid, difficulty in blowing and clenching teeth)
x Involvement of neck lymph node
x Restriction of jaw movements
Fig. 4.21: Typical parotid swelling with ear lobe raised. Facial nerve
should be tested by clenching the teeth.
Fig. 4.19: Pleomorphic adenoma showing curtain sign.
Fig. 4.22: Parotid tumour showing typical raise in earlobe
pleomorphic adenoma.
PAIN IN SALIVARY TUMOURS
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B
x Benign tumours are usually painless
x Sudden onset of pain denotes malignant transformation
x Pain is dull boring at primary site or referred to ear through
auriculotemporal nerve
x Pain is due to:
– Capsular distension by tumour
– Obstruction to free flow of saliva
– Nerve infiltration
– Inflammation like in Warthin’s
– Tumour necrosis
Investigations
FNAC is very important and diagnostic.
CT scan to know the status of deep lobe, local extension
and spread.
MRI is better method.
• Incomplete excision, 10% of tumours which are highly cellular are other
causes for recurrence.
• RT is given after surgery eventhough it is benign (controversial; a
debate).
• Inexplicable metastasis can occur even though it is benign.
• Tumour may implant due to spillage while surgical removal into retained
residual parotid (deep lobe in superficial parotidectomy).
• Recurrence after parotidectomy in pleomorphic adenoma is 5%. It is due
to spillage, improper technique, inadequate margin, retained pseudopods,
multicentricity. Recurrent tumour is multinodular without any capsule.
Expression of MUC1/DF3 in the tumour is marker to predict recurrence.
A
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CHAPTER 4 Salivary Glands
Fig. 4.23: CT picture of pleomorphic adenoma.
Note:
• Incision biopsy of parotid tumour is contraindicated as chances of seedling
and recurrence are high and also there is a chance of injuring the facial
nerve, and chance of developing parotid fistula while doing the biopsy.
• Malignant transformation in pleomorphic adenoma in early tumours is
3-5%; in long standing cases (more than 15 years) and recurrent cases
it is more than 15%.
OPEN BIOPSY IS CONTRAINDICATED IN PAROTID
B
TUMOURS DUE TO:
x Chance of injury to facial nerve
x Seedling and high chance of recurrence
x Chance of parotid fistula formation
Treatment
Surgery—first line treatment.
If only superficial lobe is involved, then superficial parot-
idectomy is done wherein parotid superficial to facial nerve
is removed.
If both lobes are involved, then total conservative parotidec-
tomy is done by retaining facial nerve.
Note:
• Enucleation is avoided as it causes high recurrence (50%) due to exten-
sion of tumour outside as pseudopods across the capsule.
B
Figs. 4.24A and B: Recurrent parotid tumour which has attained large
size. Note facial nerve is intact. Duct orifice should be inspected using
retractor.
ADENOLYMPHOMA (Warthin’s Tumour, Papillary
Cystadenoma Lymphomatosum)
It is a misnomer. It is not malignant, it is not lymphoma.
It is a benign tumour that occurs only in parotid, usually in
the lower pole.
It is said to be due to trapping of jugular lymph sacs in parotid
during developmental period.
It composed of double layer of columnar epithelium, with
papillary projections into cystic spaces with lymphoid tissues
in the stroma.
It usually involves only superficial lobe of parotid gland. It
may also be multicentric.
Smoking (40%/8 times more risk than nonsmokers) and
radiation exposure may be the cause.
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404
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Features
It presents as a slow growing, smooth, soft, cystic, fluctuant
swelling, in the lower pole, often bilateral and is nontender.
It is common in males—4:1. Common in smokers.
Common in old people—60 years.
Its incidence is 10%. Common in Whites.
It is 2nd most common benign tumour.
It is often bilateral—10%.
Investigations: Adenolymphoma produces a “hot spot” in
99
Technetium pertechnetate scan—it is diagnostic (Due to
high mitochondrial content); FNAC.
SRB's Manual of Surgery
Treatment: Superficial parotidectomy.
Note:
Adenolymphoma does not turn into malignancy. But occasionally it can
simultaneously be associated with pleomorphic adenoma, carcinoma or
lymphoma of parotid.
Fig. 4.25: Warthin’s tumour. It is seen in parotid gland usually in
superficial lobe, in lower pole.
Predilection for
99
Tc with hotspots and FNAC are the inves-
tigations.
BASAL CELL ADENOMA
It is rare, benign, now classified under monomorphic
adenoma containing isomorphic basaloid cells with basal
layer and basement membrane.
It is common in minor salivary glands; in major salivary
glands it is multicentric.
Grossly it looks like lymph node.
Microscopy—isomorphic basaloid cells with solid/trabecular/
tubular/membranous pattern.
Canalicular adenoma is its variant with bilayered ribbons of
columnar cells separated by vascular stroma.
MUCOEPIDERMOID TUMOUR
It is the commonest malignant tumour in parotid.
It is 2nd common malignant tumour in submandibular and
sublingual salivary glands.
It is commonest malignant tumour of parotid in childhood.
Incidence is 9% of salivary tumours; 20% of malignant
salivary tumours.
It occurs both in major as well as minor salivary glands.
Parotid is the commonest site; palate is the commonest minor
salivary gland site (In the palate adenoid cystic carcinoma is
common).
Radiation is the commonest etiological factor.
Gross—unencapsulated solid tumour with cystic spaces.
Microscopy—biphasic with mucin secreting (+ve for PAS,
– ve for diastase) low grade and epidermoid with high grade;
clear cell with intermediate type.
It is slowly progressive, often attains a large size and spreads
to neck lymph nodes.
It contains malignant epidermoid and mucous secreting cells.
Fig. 4.26: Warthins tumour of parotids. It is common
in males; often bilateral; common in elderly.
ONCOCYTOMA (Oxyphil Adenoma)
It is <1% of salivary tumours.
Usually benign, originating from oncocytes (oxyphilic cells).
Radiation and occupational hazards are the causes.
Common in parotid; but rarely can occur in submandibular
salivary gland.
Gross—small, tan coloured, well circumscribed encapsulated
solid tumour.
Microscopy—large oncocytes with swollen granular cyto-
plasm due to abundant mitochondria. Tyrosine crystals are
present in glandular spaces.
Fig. 4.27: Mucoepidermoid carcinoma of the parotid
with skin involvement.
Types
Low grade—mucous cells mainly—spreads to regional nodes.
Intermediate—clear cell variety
Fig. 4.28: Mucoepidermoid carcinoma of submandibular
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salivary gland.
High grade—epidermoid cells mainly—spreads to regional
nodes and also shows high propensity for distant spread.
Facial nerve involvement is late in mucoepidermoid carcinoma
of parotid.
Features
Swelling in the salivary (parotid or submandibular) region,
slowly increasing in size, eventually attaining a large size,
which is hard, nodular, often with involve ment of skin and
lymph nodes.
Common in females (3:1); slow growing.
Pain, skin and facial nerve involvement are not common
unless it is high grade.
along mandibular and maxillary divisions of trigeminal
(common) nerve and facial nerve. It infiltrates nerve more
proximally for long distance. Tumour may reach Gasserian trigeminal ganglion, pterygopalatine ganglion and
cavernous sinus.
Blood spread can occur to lungs, bones and liver. Lung
secondaries may remain dormant for many years and so is
not a contraindication for surgery of primary tumour. Blood
spread can occur decades after removal of primary tumour.
Radical parotidectomy/wide or radical excision of subman-
dibular and sublingual glands with neck nodal dissection and
postoperative RT is the treatment of choice.
Positive margin, perineural spread, solid type on microscopy
carry poor prognosis. Lung metastasis will not affect the
prognosis.
Local recurrence is common. 5-year survival is 70%.
Regional nodal spread can occur but rare.
ACINIC CELL TUMOUR
It is a rare, slow growing tumour that occurs almost always
in parotid and is composed of cells alike serous acini.
It is more common in women. It occurs in adult and elderly.
It is 3% of salivary tumours; 90% occurs in parotid.
Microscopically, it can be microcystic (commonest), papil-
lary, follicular, medullary etc.
It can involve facial nerve or neck lymph nodes.
Clinically, it is of variable consistency with soft and cystic
areas.
It is low grade malignant tumour.
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CHAPTER 4 Salivary Glands
ADENOID CYSTIC CARCINOMA
(10% of
It is most common tumour in submandibular and sublin-
gual salivary glands. 50% of cases occur in minor salivary
glands—palate.
It is also called as cylidromatous carcinoma.
It is 2nd most common malignant salivary tumour; but it is
rare in parotid (2% of parotid tumours, 15% of malignant
parotid tumours.
It is common in females (3:2). Common in 5th and 6th
decades.
It is slow growing but highly malignant with remarkable
capacity for recurrence. But it is classified under low grade
malignancy.
Microscopy: Cribriform, tubular, and solid are 3 types. Cribri-
form type shows cells in nests separated by round or oval
spaces—‘Swiss-cheese’ pattern. Myo and duct epithelial cells
with lace like pattern are also seen. It invades periosteum and
bone medulla early and spreads extensively.
It has got high affinity for perineural spread (both axially
and circumferentially; antegrade and retrograde fashion)
Salivary Tumours)
MALIGNANT MIXED TUMOUR (MMT)
It is 10% of salivary malignancy in incidence with epithelial
and mesenchymal elements.
It carries worst prognosis.
Types
Carcinoma ex pleomorphic adenoma: It is the commonest
type. Previous long standing parotid swelling shows rapid
change, fixity, facial nerve spread, neck nodal involvement are
typical. Transformation is 2% in tumour of 5 years duration;
10% in 15 years tumour. It is the most aggressive salivary
malignancy. Radical parotidectomy is the treatment.
Primary malignant mixed tumour: It is also called as carcino-
sarcoma which arises as de novo. It shows components of
both carcinoma and sarcoma with metastatic potential both
through lymph nodes and blood.
Metastasizing mixed tumours: It contains structures typical
of benign mixed tumour both at original and at metastases
sites.
In situ non-invasive carcinoma in pleomorphic adenoma:
There is no evidence of capsular invasion. Lesion with less
Nothing comes from without; all things come from within.
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