IN THE NAME OF GOD

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IN THE NAME OF GOD
Salivary Glands Dr.S.A.Mirvakili
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Anatomy and Physiology of the Salivary Glands
The Major Salivary Glands - Parotid -
Submandibular - Sublingual The Minor Salivary
Glands
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Anatomy Parotid Gland

• Nearly 80 of the parotid gland (PG) is found
  below the level of the external auditory canal,
  between the mandible and the SCM.
• Superficial to the posterior aspect of the
  masseter mm

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• CN VII branches roughly divide the PG into
  superficial and deep lobes while coursing
  anteriorly from the stylomastoid foramen to the
  muscles of facial expression.

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Anatomy Parotid Duct

• Small ducts coalesce at the anterosuperior aspect
  of the PG to form Stensens duct.
• Runs anteriorly from the gland and lies
  superficial to the masseter muscle
• Follows a line from the EAM to a point just above
  the commissure.
• Is inferior to the transverse facial artery
• It is 1-3 mm in diameter
• 6cm in length

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• At the anterior edge of the masseter muscle,
  Stensens duct turns sharply medial and passes
  through the buccinator muscle, buccal mucosa and
  into the oral cavity opposite the maxillary
  second molar.

Anatomy Parotid Fascia

• Gland encapsulated by a fascial layer that is
  continuous the deep cervical fascia (DCF).
• The stylomandibular ligament (portion of the DCF)
  separates the parotid and submandibular gland.

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Parotid Parasympathetic Innervation

• Preganglionic parasympathetic (from CN9) arrives
  at otic ganglion via lesser petrosal n.
• Postganglionic parasympathetic leaves the otic
  ganglion and distributes to the parotid gland via
  the auriculotemporal nerve.

ParotidSympathetic Innervation

• Postganglionic innervation is provided by the
  superior cervical ganglion and distributes with
  the arterial system

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AnatomySubmandibular gland

• Located in the submandibular triangle of the
  neck, inferior lateral to mylohyoid muscle.
• The posterior-superior portion of the gland
  curves up around the posterior border of the
  mylohyoid and gives rise to Whartons duct.

Anatomy Submandibular Duct
Whartons duct passes forward along the superior
surface of the mylohyoid adjacent to the lingual
nerve. Between Mylohyoid Hyoglossus 5 cm in
length ,2-4mm in diameter
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AnatomySubmandibular gland

• Innervation
• Superior Cervical Ganglion (symp)
• Submandibular Ganglion (para)
• Artery Submental branch of Facial a.
• Vein Anterior Facial vn.
• Lymphatics Deep Cervical and Jugular chains
• Facial artery nodes

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Submandibular duct
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Anatomy Sublingual glands

• Lie on the superior surface of the mylohyoid
  muscle and are separated from the oral cavity by
  a thin layer of mucosa.

• The ducts of the sublingual glands are called
  Bartholins ducts.
• In most cases, Bartholins ducts consists of 8-20
  smaller ducts of Rivinus. These ducts are short
  and small in diameter.

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Anatomy Sublingual glands

• Between Mandible Genioglossus
• No capsule
• Ducts of Rivinus /- Bartholins duct
• Sialogram not possible
• Innervation Same as Submandibular
• Artery/Vein Sublingual branch of Lingual
  Submental branch of Facial
• Lymphatics Submandibular nodes

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Salivary Gland Infections

• Acute bacterial sialdenitis
• Chronic bacterial sialdenitis
• Viral infections

• Sialadenitis represents inflammation mainly
  involving the acinoparenchyma of the gland.

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Sialadenitis

• Acute infection more often affects the major
  glands than the minor glands1

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Pathogenesis

• 1. Retrograde contamination of the salivary ducts
  and parenchymal tissues by bacteria inhabiting
  the oral cavity.
• 2. Stasis of salivary flow through the ducts and
  parenchyma promotes acute suppurative infection.

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Acute Suppurative

• More common in parotid gland.
• Suppurative parotitis, surgical parotitis,
  post-operative parotitis, surgical mumps, and
  pyogenic parotitis.
• The etiologic factor most associated with this
  entity is the retrograde infection from the
  mouth.
• 20 cases are bilateral7

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Risk Factors for Sialadenitis

• Systemic dehydration (salivary stasis)
• Chronic disease and/or immunocompromise
• Liver failure
• Renal failure
• DM, hypothyroid
• Malnutrition
• HIV
• Sjögrens syndrome

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Risk Factors continued

• Neoplasms (pressure occlusion of duct)
• Sialectasis (salivary duct dilation) increases
  the risk for retrograde contamination. Is
  associated with cystic fibrosis and
  pneumoparotitis
• Extremes of age
• Poor oral hygiene
• Calculi, duct stricture
• NPO status (stimulatory effect of mastication on
  salivary production is lost)

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Acute Suppurative Parotitis - History

• Sudden onset of erythematous swelling of the
  pre/post auricular areas extend into the angle of
  the mandible.
• Is bilateral in 20.

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Bacteriology

• Purulent saliva should be sent for culture.
• Staphylococcus aureus is most common
• Streptococcus pnemoniae and S.pyogenes
• Haemophilus Influenzae also common

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Lab Testing

• Parotitis is generally a clinical diagnosis
• However, in critically ill patients further
  diagnostic evaluation may be required
• Elevated white blood cell count
• Serum amylase generally within normal
• If no response to antibiotics in 48 hrs can
  perform MRI, CT or ultrasound to exclude abscess
  formation
• Can perform needle aspiration of abscess

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Treatment of Acute Sialadenitis

• Reverse the medical condition that may have
  contributed to formation
• Discontinue anti-sialogogues if possible
• Warm compresses, maximize OH, give sialogogues
  (lemon drops)
• External salivary gland massage if tolerated

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Treatment of Acute Sialadenitis/Parotitis

• Antibiotics!
• 70 of organisms produce B-lactamase or
  penicillinase
• Need B-lactamase inhibitor like Augmentin or
  Unasyn or second generation cephalosporin
• Can also consider adding metronidazole or
  clindamycin to broaden coverage

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Surgery for Acute Parotitis

• Limited role for surgery
• When a discrete abscess is identified, surgical
  drainage is undertaken
• Approach is anteriorly based facial flap with
  multiple superficial radial incisions created in
  the parotid fascia parallel to the facial nerve
• Close over a drain

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Chronic Sialadenitis

• Causative event is thought to be a lowered
  secretion rate with subsequent salivary stasis.
• More common in parotid gland.
• Damage from bouts of acute sialadenitis over time
  leads to sialectasis, ductal ectasia and
  progressive acinar destruction combined with a
  lymphocyte infiltrate.

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Chronic Sialadenitis

• Of importance in the workup
• The clinician should look for a treatable
  predisposing factor such as a calculus or a
  stricture.

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Acute viral infection (AVI)

• Mumps classically designates a viral parotitis
  caused by the paramyxovirus
• However, a broad range of viral pathogens have
  been identified as causes of AVI of the salivary
  glands.

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Viral Infections

• As opposed to bacterial sialadenitis, viral
  infections of the salivary glands are SYSTEMIC
  from the onset!

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Virology

• Classic mumps syndrome is caused by
  paramyxovirus, an RNA virus
• Others can cause acute viral parotitis
• Coxsackie A B, ECHO virus, cytomegalovirus and
  adenovirus
• HIV involvement of parotid glands is a rare cause
  of acute viral parotitis, is more commonly
  associated with chronic cystic dz

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Clinical presentation

• 30 experience prodromal symptoms prior to
  development of parotitis
• Headache, myalgias, anorexia, malaise
• Onset of salivary gland involvement is heralded
  by earache, gland pain, dysphagia and trismus

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Physical exam

• Glandular swelling (tense, firm) Parotid gland
  involved frequently, SMG SLG can also be
  affected.
• May displace ispilateral pinna
• 75 cases involve bilateral parotids, may not
  begin bilaterally (within 1-5 days may become
  bilateral).25 unilateral
• Low grade fever

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Treatment

• Supportive
• Fluid
• Anti-inflammatories and analgesics

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Complications

• Orchitis, testicular atrophy and sterility in
  approximately 20 of young men
• Oophoritis in 5 females
• Aseptic meningitis in 10
• Pancreatitis in 5
• Sensorineural hearing loss lt5
• Usually permanent
• 80 cases are unilateral

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Immunologic Disease
Sjögrens Syndrome

• Most common immunologic disorder associated with
  salivary gland disease.
• Characterized by a lymphocyte-mediated
  destruction of the exocrine glands leading to
  xerostomia and keratoconjunctivitis sicca

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Sjögrens syndrome

• 90 cases occur in women
• Average age of onset is 50y
• Classic monograph on the disease published in
  1933 by Sjögren, a Swedish ophthalmologist

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Sjögrens Syndrome

• Two forms
• Primary involves the exocrine glands only
• Secondary associated with a definable autoimmune
  disease, usually rheumatoid arthritis.
• 80 of primary and 30-40 of secondary involves
  unilateral or bilateral salivary glands swelling

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Sjögrens Syndrome

• Unilateral or bilateral salivary gland swelling
  occurs, may be permanent or intermittent.
• Rule out lymphoma

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Sjögrens Syndrome

• Keratoconjuntivitis sicca diminished tear
  production caused by lymphocytic cell replacement
  of the lacrimal gland parenchyma.
• Evaluate with Schirmer test. Two 5 x 35mm strips
  of red litmus paper placed in inferior fornix,
  left for 5 minutes. A positive finiding is
  lacrimation
• of 5mm or less.
• Approximately 85 specific sensitive

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Sjögrens Treatment

• Avoid xerostomic meds if possible
• Avoid alcohol, tobacco (accentuates xerostomia)
• Sialogogue (egpilocarpine) use is limited by
  other cholinergic effects like bradycardia
  lacrimation
• Sugar free gum or diabetic confectionary
• Salivary substitutes/sprays

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Sialadenosis

• Non-specific term used to describe a
  non-inflammatory non-neoplastic enlargement of a
  salivary gland, usually the parotid.
• May be called sialosis
• The enlargement is generally asymptomatic
• Mechanism is unknown in many cases.

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Related to

• Metabolic endocrine sialendosis
• Nutritional nutritional mumps
• Obesity secondary to fatty hypertrophy
• Malnutrition acinar hypertrhophy
• Any condition that interferes with the absorption
  of nutrients (celiac dz, uremia, chronic
  pancreatitis, etc)

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Related to

• Alcoholic cirrhosis likely based on protein
  deficiency resultant acinar hypertrophy
• Drug induced iodine
• Mumps
• HIV

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Granulomatous Disease

• Primary Tuberculosis of the salivary glands
• Uncommon, usually unilateral, parotid most common
  affected
• Believed to arise from spread of a focus of
  infection in tonsils
• Secondary TB may also involve the salivary glands
  but tends to involve the SMG and is associated
  with active pulmonary TB.

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• Sarcoidosis a systemic disease characterized by
  noncaseating granulomas in multiple organ systems
• Clinically, SG involvement in 6 cases
• Heerfordtss disease is a particular form of
  sarcoid characterized by uveitis, parotid
  enlargement and facial paralysis. Usually seen in
  20-30s. Facial paralysis transient.

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• Cat Scratch Disease
• Does not involve the salivary glands directly,
  but involves the periparotid and submandibular
  triangle lymph nodes
• May involve SG by contiguous spread.
• Bacteria is Bartonella Henselae(G-R)
• Also, toxoplasmosis and actinomycosis.

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Sialolithiasis

• The exact pathogenesis of sialolithiasis remains
  unknown.
• Thought to form via.
• an initial organic nidus that progressively
  grows by deposition of layers of inorganic and
  organic substances.
• May eventually obstruct flow of saliva from the
  gland to the oral cavity.

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• Acute ductal obstruction may occur at meal time
  when saliva producing is at its maximum, the
  resultant swelling is sudden and can be painful.
• Gradually reduction of the swelling can result
  but it recurs repeatedly when flow is stimulated.
  
• This process may continue until complete
  obstruction and/or infection occurs.

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Etiology

• Water hardness ?likelihood? Maybe.
• Hypercalcemiain rats only
• Xerostomic meds
• Tobacco smoking, positive correlation
• Smoking has an increased cytotoxic effect on
  saliva, decreases PMN phagocytic ability and
  reduces salivary proteins
• Gout is the only systemic disease known to cause
  salivary calculi and these are composed of uric
  acid.

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Stone Composition

• Organic often predominate in the center
• Glycoproteins
• Mucopolysaccarides
• Bacteria!
• Cellular debris
• Inorganic often in the periphery
• Calcium carbonates calcium phosphates in the
  form of hydroxyapatite

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Reasons sialolithiasis may occur more often in
the SMG

• Saliva more alkaline
• Higher concentration of calcium and phosphate in
  the saliva
• Higher mucus content
• Longer duct
• Anti-gravity flow

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Other characteristics

• Despite a similar chemical make-up,
• 80-90 of SMG calculi are radio-opaque7
• 50-80 of parotid calculi are radiolucent7
• 30 of SMG stones are multiple
• 60 of Parotid stones are multiple

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Clinical presentation

• Painful swelling (60)
• Painless swelling (30)
• Pain only (12)
• Sometimes described as recurrent salivary
• colic and spasmodic pains upon eating

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Diagnostics Plain occlusal film

• Effective for intraductal stones, while.
• intraglandular, radiolucent or
• small stones may be missed.

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Diagnostic approach Diagnostic Sialendoscopy2

• Allows complete exploration of the ductal system,
  direct visualization of duct pathology
• Success rate of gt952
• Disadvantage technically challenging, trauma
  could result in stenosis, perforation

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Sialolithiasis Treatment

• None antibiotics and anti-inflammatories,
  hoping for spontaneous stone passage.
• Stone excision
• Lithotripsy
• Interventional sialendoscopy
• Simple removal (20 recurrence)7
• Gland excision

• If patients DO defer treatment, they need to
  know
• Stones will likely enlarge over time
• Seek treatment early if infection develops
• Salivary gland massage and hyper-hydration when
  symptoms develop.

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Transoral vs. Extraoral Removal

• Some say
• if a stone can be palpated thru the mouth, it can
  be removed trans-orally (TO)
• Or if it can be visualized on a true central
  occlusal radiograph, it can be removed (TO).
• Finally, if it is no further than 2cm from the
  punctum, it can be removed (TO).

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Gland excision indicated

• Very posterior stones
• Intra-glandular stones
• Significantly symptomatic patients
• Failed
• transoral
• approach

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Thanks for your attention