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Examination of Salivary Gland
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Causes for submandibular sialadenitis Types of sialadenitis
Bacterial – more common. It is usually due to Acute
obstruction and stasis • Bacterial—occurs in submandibular salivary ductal
Trauma over duct causing oedema / stricture and stasis obstruction (Wharton’s) or in parotid gland. In parotid
Viral – mumps – rare 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
Note: Salivary colic can be induced by meals, lemon juice, etc. Irritation of the lingual nerve, which is in very close
proximity to submandibular salivary duct, causes referred pain in tongue – lingual colic.
291
Sialectasis
It is an aseptic dilatation of salivary ductules causing
grape-like (cluster like) dilatations. It is a disease of
unknown etiology with destruction of parenchyma of
gland accompanied by stenosis and cyst formation
in the ducts. It is common in parotids; often bilateral;
presents as a smooth, soft, fluctuant, nontransillu-
between 3-6 years without any known etiology.
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.
minating swelling which increases in size during
mastication. It is tender initially . It lasts for many days
with a long symptom free period of the disease.
Sialogram is diagnostic (grape cluster look).
Parotid Abscess (Suppurative Sialadenitis)
It is a result of an acute bacterial sialadenitis of parotid
gland. It is an ascending bacterial parotitis, due to
reduced salivary flow and poor oral hygiene. Causative
Recurrent Childhood Parotitis
It is a recurrent, rapid enlargement of one or both
parotids with fever and malaise in children of age group
Causes of acute parotitis (Differential diagnosis of Complications of parotid abscess
suppurative parotitis)
Viral—Mumps (commonest cause of parotitis), Coxsackie virus A and B, Septicaemia
parainfluenza 1 and 3, Echo and lymphocytic choriomeningitis Severe trismus
Bacterial – Staphylococcus aureus Dysphagia
Allergic; HIV infection Rupture into external auditory canal
Radiotherapy, postoperative period
Specific infections like syphilis
Sjogren’s syndrome often causing bilateral parotitis Chronic parotitis
Features of acute parotitis Stenson’s duct presenting as rubbery
Continuous, throbbing pain radiating to ear and side hard slightly tender recurrent swelling
of the head; speaking/eating/any movements in parotid region which is more during
of TM joint is painful eating, with aching pain. Often it may
Fever with chills and rigors be bilateral.
Diffuse swelling in front and behind the ear which is tender smooth
firm with brawny induration, redness and warmness; it is nonmobile
becomes prominent by clinching teeth
Neck upper deep nodes may be tender and enlarged
Restricted TM joint mobility; trismus
Facial nerve is normal
Oedematous ductal orifice with often discharge is common
organisms are Staphylococcus aur eus, S treptococcus
viridans, and often others like gram-negative and
anaerobic organisms. It is an ascending bacterial
It can occur due to stone blocking the
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Remember about salivary fistula
Commonly from the parotid
It can be internal draining into the mouth or can be external draining outside
It is acquired commonly but rarely can be congenital
It can be due to surgery, trauma or due to sepsis
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
Fistula due to ductal disruption leaks profusely and invariably needs surgery to close it
Submandibular gland fistula commonly closes spontaneously, rarely if not, requires complete removal of the gland
Anticholinergics, irradiation, denervation of the gland, duct ligation are done to reduce saliva production
Excision of fistula, repair of the duct, diversion of the duct into the mouth are other options
In severe intractable cases, removal of the gland/total conservative parotidectomy is needed
SRB’s Clinical Surgery
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.
Clinical features: Pyrexia, malaise, pain, trismus; firm
swelling is seen in the parotid region which is red,
tender, warm, well localised, tender lymph nodes are
palpable in 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 parotid region; Pus collected
from duct orifice is sent for culture and sensitivity;
Needle aspiration from the abscess to confirm the
formation of pus; Sialogram is contraindicated in acute
phase, as it will cause retrograde infection leading
into bacteraemia. Note: In suppurative parotitis patient
may develop severe laryngeal or pharyngeal oedema
and may require steroids, tracheostomy and critical
care.
Parotid Fistula
Parotid fistula may arise from parotid gland or duct
or ductules. It may open inside the mouth as internal
fistula; or open outside onto the skin as external fistula
(Fig. 12.37). Fistula from the duct has profuse
discharge. Fistula from the gland often shows only
minimal discharge.
Causes: After superficial parotidectomy; after drainage of parotid abscess; trauma; malignant recurrence
of tumour.
Clinical features: Discharging fistula in the parotid
region of face; tenderness and induration; trismus.
Fig. 12.37: Parotid fistula.
Diagnosis: Fistulogram. Sialography to find out the
origin of the fistula whether from parotid gland or
duct or ductules; discharge study; MRI.
Sjogren’s Syndrome (Tage Sjogren,
Swedish Physician 1939)
It is an autoimmune disease causing progressive des-
truction of salivary and lacrimal glands, leading to
keratoconjunctivitis sicca (dry eyes) and xeroph-
thalmia (dry mouth). Types: 1. Primary, 2.
Secondary. Secondary Sjogren’s syndrome: Dry
mouth; Dry eyes; W ith association of connective tissue
disorders like primary biliary cirrhosis (near 100%);
SLE (30%); Rheumatoid arthritis (15%). Female to
male ratio is 10:1.
Primary Sjogren’s syndrome: Severe dry mouth;
Severe dry eyes; W idespread dysfunction of exocrine
glands; incidence of developing lymphomas is high;
there is no association of connective tissue disorders.
Examination of Salivary Gland
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Clinical Features
It is common in middle aged females who present
with dry eyes, dry mouth, enlarged parotids and enlarged lacrimal glands; often they are tender; superadded
infection of the mouth with, Candida albicans is
common. Sjogren’s syndrome often causes bilateral
parotitis.
Investigations
Autoantibody estimation–Rheumatoid factor, 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
pertechnatate scan for gland function.
Mikulicz Disease
It is a clinical variant of Sjogren’s syndrome. It is
an autoimmune disorder of salivary and lacrimal
glands, resulting in infiltration of the glands with round
cells. Glandular tissue is replaced by lymphocytes.
293
A
Triad: (1) Symmetrical and progressive enlargement
of all salivary glands (parotid, submandibular, sublingual, accessory parotid). (2) Narrowing of palpebral
fissures due to enlargement of the lacrimal glands.
(3) Parchment-like dryness of the mouth but patient
is not thirsty.
Heerfordt’s Syndrome
It is sarcoidosis of parotid swelling; anterior uveitis;
facial palsy and fever.
Anatomy of Parotid Gland (Para-around, Otis-ear)
Parts of the Parotid Gland
Superficial part (80%) - lies over the posterior part
of the ramus of mandible. Deep part lies behind the
mandible and medial pterygoid muscle. Parotid gland
is pyramidal shaped with upper pole just below the
zygomatic bone and wedged between external auditory
meatus and the mandibular joint. Anterior border is
over the masseter; lower pole is below and behind
the angle of the mandible and indented by sternomastoid. Parotid is covered by dense parotid fascia
which is derived from investing layer of deep fascia
(Figs 12.38A and B). Accessory parotid is prolon-
B
Figs 12.38A and B: Anatomical
relations of the parotid gland.
gation of the gland along the parotid duct. Parotid
(Stensen’s) duct is 2-3 mm in diameter, emerges from
the anterior border of the gland runs horizontally across
masseter and passes through the buccinator muscle
and opens into the oral mucosa opposite upper second
molar tooth (Fig. 12.39). Facial nerve emerges from
the stylomastoid foramen lying between external
auditory meatus and mastoid process. It passes around
the neck of the condyle of mandible and becomes
superficial, later dividing into temporofacial and
cervicofacial branches which in turn divides into many
branches. Some of these may be interconnected as
pes anserinus(goose foot) (Fig. 12.40). Branches are
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SRB’s Clinical Surgery
Fig. 12.39: Accessory parotid tumour. It contains both
serous and mucous acini.
– temporal (auricularis anterior and superior part of
frontalis), zygomatic (frontalis and orbicularis oculi),
upper buccal and lower buccal (buccinator, orbicularis
oris, elevators of the lip). mandibular (lower lip
muscles) and cervical (platysma) (Fig. 12.41).
Blood supply is from external carotid artery; venous
drainage is to external jugular vein. Nerve supply is
Fig. 12.40: Facial nerve distribution – Pes anserinus.
from autonomic nervous system; parasympathetic is
secretomotor from auriculotemporal nerve; sympathe-
tic is vasomotor from plexus around external carotid
artery. Faciovenous plane of Patey of retromandibular
vein is of surgical importance as facial nerve branches
lie superficial to it. 25% of saliva is from parotids.
Fig. 12.41: Patey’s vascular plane in parotid.
Examination of Salivary Gland
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Structures within the parotid gland from deep to
superficial–
External carotid artery, maxillary artery, superficial
temporal artery, posterior auricular artery
Retromandibular vein (by maxillary and superficial temporal
veins)
Facial nerve with its branches.
Great auricular nerve (cutaneous sensory around
angle and lower part of the ear lobule) and auriculotemporal nerve which is from mandibular division of
trigeminal nerve (secretomotor to parotid gland) are
other nerves present in relation to parotid gland.
Secretomotor Fibres
Secretomotor preganglionic fibres from inferior
salivary nucleus → glossopharyngeal nerve →
tympanic branch → tympanic plexus → lesser
superficial petrosal nerve → otic ganglion → postganglionic fibres → auriculotemporal nerve, branch
of mandibular division of trigeminal nerve → parotid
gland.
Parotid gland is serous. Submandibular gland is
mixed (major is mucous). Sublingual is mucous. Minor
salivary glands are mucous except von Eber’ s glands
which empty into the circumvallate papillae and glands
in the tongue tip.
295
A
SUBMANDIBULAR SALIVARY GLAND
Parts
Superficial part lies in submandibular triangle,
superficial to mylohyoid and hyoglossus muscles,
between the two bellies of digastric muscles. Deep
part is in the floor of the mouth and deep to the
mylohyoid. Submandibular (Wharton’s) duct (5 cm),
comes from the deep part of the gland, enters the floor
of the mouth, on a papilla beside the frenum of the
tongue. Lingual nerve and submandibular ganglion
are attached to upper pole of the gland. Facial artery
emerges from under surface of the stylohyoid muscle,
enters the gland from posterior and deep surface
reaching its lateral surface crossing the lower border
of mandible to enter the face. Venous drainage is to
anterior facial vein. 70% of total saliva is from
submandibular salivary gland (Figs 12.42A and B).
Resting salivary flow usually arises from the
submandibular salivary gland. Sialorrhoea is increased
B
Figs 12.42A and B: Anatomical relations of the
submandibular salivary gland.
salivary flow often seen due to drugs, in cerebral palsy,
physically handicapped person, children, and
psychiatry patients. Intractable sialorrhoea can be
corrected by different surgeries to submandibular
salivary gland like duct repositioning to excision of
the gland. Normal salivary secretion per day is
1500 ml. It is hypotonic fluid with pH 7.0. It contains
α amylase.
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Xerostomia is decreased salivary flow. It is seen
in post-menopausal women, depression, dehydration,
use of antidepressant drugs; anticholinergic drugs,
Sjogren’s syndrome, radiotherapy to head and neck
region.
Secretomotor Fibres of Submandibular
Salivary Gland
Preganglionic fibres from superior salivary nucleus
→ facial nerve → chorda tympani nerve → lingual
nerve → submandibular ganglion → post-ganglionic
fibres → submandibular and sublingual salivary
glands.
Minor Salivary Glands
There are around 450 minor salivary glands which
are distributed in lips, cheeks, palate and floor of the
mouth. Glands also may be present in oropharynx,
larynx, trachea and paranasal sinuses. They contribute
to 10% of total salivary volume. Sublingual salivary
glands are minor salivary glands one on each side;
located in the anterior aspect of the floor of the mouth
in relation to mucosa, mylohyoid muscle, body of the
mandible near mental symphysis (Fig. 12.43). Gland
drains directly into mucosa or through a duct which
drains into submandibular duct. This duct is called
as Bartholin duct. Mikulicz’s disease is common in
sublingual salivary gland. Minor salivary glands are
not present in gingivae and anterior portion of the
hard palate.
Fig. 12.43: Swelling in sublingual region.
Ectopic Salivary Gland
Ectopic salivary gland also called as aberrant salivary
gland / migrant salivary gland is nothing but ectopic
lobe of the juxtaposed salivary gland. It is commonly
seen in relation to submandibular salivary gland.
Commonest ectopic salivary tissue is Stafne bone cyst.
It is invagination of the juxtaposed submandibular
salivary gland into the mandible bone on its lingual
aspect. X-ray shows radiolucent area due to the cyst
below the angle of the mandible, lower to inferior
dental vessels and nerve. Jaws, eyelids, middle ear,
paranasal sinus, nose, rarely skin of face and neck
are other sites wherein ectopic salivary tissue can be
demonstrated.
Examination of Neck
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Examination of
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13
Neck is a complex anatomical area comprised of many
compartments, triangles, tubes (trachea, oesophagus),
vessels and lymph nodes. Thorough anatomical
knowledge of the area is essential for safe clinical
and surgical practice. Student should read the specific
anatomical book for the same.
History taking begins with:
Name:
Age:
Occupation:
Address:
Sex:
Cystic hygroma, branchial cyst and fistula are congenital in origin. Sternomastoid tumour , a misnomer
seen in infants and children, due to organised haematoma in sternomastoid muscle leading to fibrosis of
its muscle fibres following a birth trauma. Tuberculous
lymphadenitis occurs in young adults; carcinoma
secondaries in lymph nodes usually occur in elderly.
Neck
malignant. Malignancy may be lymph node secondaries or lymphoma. It takes few months for tuberculous cold abscess to evolve in a tuberculous
lymphadenitis. Presence of similar swelling elsewhere
in the body like in axilla, abdomen, and groin suggests
that it could be lymphoma.
Pain: Time of onset of pain, whether it was present
at the beginning,whether initially painless later became
painful (sepsis, infiltration, tumour necrosis). Acute
conditions are painful to start. Malignancy is initially
painless.
Fever: Fever suggests acute inflammatory condition;
mild fever with occasionally evening rise is seen in
tuberculous lymphadenitis. But one should remember
that fever is not necessarily a feature in all patients
with many tuberculous lymphadenitis.
Relevant histories like cough, haemoptysis (tuberculosis, lymphoma, and carcinoma), voice change, dyspnoea, dysphagia, abdominal discomfort are important
to be noted.
History
History of Present Illness
Swelling: Swelling is the commonest presentation in
the neck. Lymph nodal mass is the commonest type
of swelling in the neck. It could be due to lymphadenitis
(nonspecific bacterial infection and inflammation);
tuberculosis; malignancy; AIDS, viral causes. Other
swellings which can occur in the neck are cystic
swellings, carotid body tumour, cervical rib, carotid
aneurysm, etc. History (like in chapter swelling) should
be asked in detail. History associated with onset,
progress, duration, recent increase in size, number,
etc. should be asked. Acute inflammatory swellings
are of very short duration with signs of acute
inflammation. Swelling of short duration is commonly
Past History
Past history of treatment for tuberculosis, their details,
treatment for malignancy (surgery, chemotherapy,
radiotherapy) are important points should be asked.
Personal History
History of smoking, alcohol consumption, dietary
habits, decreased appetite and loss of weight (in advanced carcinoma lymphoma and in tuberculosis) should
be asked.
General Examination
Anaemia, clubbing, jaundice are checked. Pulse and
blood pressure are recorded, nutrition and built are
assessed.
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Local Examination
Inspection
Neck should be examined with proper exposure upto
the nipples. Entire neck including all triangles should
be examined (Fig. 13.1).
Fig. 13.1: Proper inspection of the neck is essential.
Swelling: Swelling is the commonest presentation in
the neck. Lymph nodes are the commonest of the neck
swellings. Its number, site, size, shape, extent, surface,
dilated veins, skin changes like redness, oedema,
ulceration or fungation should be inspected. Branchial
cyst is located at the level of upper 1/3rd and middle
1/3rd of the sternomastoid muscle with posterior ½
of the swelling lying under the sternomastoid muscle.
Lymph nodes can get enlarged in any area in neck.
Surface is nodular in secondaries and tuberculosis,
smooth in lymphoma. Cold abscess shows smooth
surface on inspection. Ranula can occur in upper neck.
Dermoid cyst can occur in chin, in space of Burns
in midline. Cervical rib, cystic hygroma, subclavian
artery aneurysm occur in posterior triangle of the neck.
Carotid artery aneurysm is seen usually in carotid
triangle or along the line of carotid artery. Carotid
body tumour is seen in carotid triangle. Swelling should
be differentiated from thyroid swelling by checking
movement with deglutition. Thyroid swelling, thyroglossal cyst, subhyoid bursa all move with deglutition.
Skin over the swelling is looked for— dilated veins,
redness (inflammation), oedema (inflammation or
malignancy), discharging sinus/fistula, ulcer, scar.
Branchial fistula is located in junction of middle
1/3rd and lower 1/3rd of the sternomastoid muscle
along the anterior margin; thyr oglossal fistula in the
midline lower 1/3rd; tuberculous sinus can occur in
the neck, the site depends on the location of the
underlying tuberculous lymphadenitis, undermined
tuberculous ulcer is known to occur; chronic pyogenic
osteomyelitis of the mandible can cause discharging
sinus over the lower margin of the mandible; actinomycosis of mandible causes multiple sinuses with
discharge containing sulphur granule; syphilitic
gummatous ulcer may be seen in sternomastoid muscle
(now rare). Sinus, ulceration, fungation may be features
of advanced fixed secondaries in the lymph node.
W asting of trapezius, sternomastoid, and other neck
muscles should be noted, torticollis (chin turns towards
opposite side and neck towards same side due to spasm/
contraction/fibrosis of sternomastoid muscle); dilated
veins in neck, and chest wall suggest mediastinal
compression by tumour/nodes. In torticollis, face is
often less developed on the affected side. When patient
attempts to straighten the neck, sternal head of
sternomastoid stands out taut and firm with inability
to straighten the head. Asymmetry of skull can be
detected by examining the head and neck from behind.
All swellings should be inspected carefully with
relation to sternomastoid muscle.
Palpation
Palpation of neck is done with patient sitting on a
stool and examiner standing behind the patient. First
always ascertain the relation of the swelling to
sternomastoid by palpation. W ith examiner standing
behind the patient, patient is asked to push his chin
against examiner’s hand firmly to make the sternomastoid muscle tense; with the other hand examiner
should palpate the sternomastoid muscle from below
upward along its anterior border and ascertain the
swelling in relation to the muscle (Fig. 13.2).
Cervical lymph nodes are also examined from
behind. Patient should flex the neck to relax the muscle
and fascia to make the swelling better for palpation.
Usual order of lymph nodes are Levels I, II, III, IV,
V and VI. Submandibular group of nodes are felt with
neck flexed towards same side. In posterior triangle
both supraclavicular and suboccipital nodes should
Examination of Neck
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Fig. 13.2: Method of checking the relation of sternomastoid
muscle to swelling by palpating from behind.
be palpated. Often supraclavicular lymph nodes are
palpated from front. V ir chow’s node between the two
heads of the sternomastoid is palpated from front.
Swelling should be palpated for location, size, shape,
surface, consistency, mar gin, reducibility, impulse on
coughing, and mobility. Tuberculosis causes matted
lymph nodes; secondaries cause stony hard nodular
swelling; lymphoma causes India rubber-like firm
swelling (Figs 13.3 and 13.4A and B).
299
A
Fig. 13.3: Hodgkin’s lymphoma neck both sides.
It is India rubber-like firm in consistency.
B
Figs 13.4A and B: Secondaries in neck nodes – nodular
surface, stony hard consistency are typical.
Plane of the swelling is checked by contracting
the sternomastoid against resistance by turning the
chin opposite side (against the resistance of the
examiner’s hand). Examiner’s hand is placed under
the chin of the patient; who is asked to push/nod the
chin downwards against resistance of examiner’s hand
and swelling is palpated to check whether it is deep
to sternomastoid or not and the plane is checked on
both sides simultaneously . If swelling is in deeper plane,
it reduces in size with restricted mobility when muscle
is made taut. If swelling is in superficial plane, it
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A
C
Figs 13.5A to D: Skin pinching (for fixity); mobility; contraction of sternomastoid against resistance towards
opposite side to find out the plane of the swelling; palpation from all directions of the swelling are essential.
D
becomes more prominent after muscle contraction and
still mobile over the muscle (Figs 13.5A to D).
Swelling will be completely immobile if it is fixed
posteriorly to paravertebral region as seen in advanced
secondaries in neck.
Pinching the skin/gliding the skin over the swelling
should be done to assess the fixity to skin. It can be
B
often fixed to swelling in secondaries/tuberculosis
forming collar stud abscess and acute lymphadenitis
(Figs 13.6A to C).
Pulsation: Expansile/transmitted, fluctuation (in two
directions)/Paget’s test; transillumination (like in other
swelling) should be checked. Cold abscess, cystic
hygroma, lymph cyst, branchial cyst, dermoid cyst,
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