Inflammation of salivary gland

Risk factors:

• Systemic dehydration (salivary stasis)
• Chronic disease and/or immunocompromise
  • Liver failure
  • Renal failure
  • DM
  • Hypothyroid
  • Malnutrition
  • HIV
  • Sjögren’s syndrome
• 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)
• Sialolithiasis – mechanical obstruction of the duct resulting in salivary stasis and subsequent gland infection

Pathology:

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 infection

More common in parotid gland

• Etiology: the retrograde infection from the mouth
• 20% cases are bilateral
  • Suppurative parotitis
  • Surgical parotitis
  • Post-operative parotitis
  • Surgical mumps
  • Pyogenic parotitis
• Predilection for parotid: Parotid is primarily serous

• Differentials for parotid gland enlargement:
  • Lymphoma
  • Actinomycoses
  • Cat-scratch disease
  • Sjogren’s syndrome
  • Wegener’s granulomatosis
  • Viral infection

NB: Calculus formation is more likely to occur in submandibular gland duct (85-90% of salivary calculi are in the SMG duct) However, the parotid gland remains the most common site of acute suppurative infection

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Bacterial sialadenitis

Pathology:

• Mucoid saliva contains lysozymes & IgA antibodies – protect against bacterial infection (therefore, parotid has ↓ bacteriostatic activity)
• Mucins contain sialic acid – which agglutinates bacteria and prevents its adherence to host tissue
• Specific glycoproteins in mucins bind epithelial cells competitively inhibiting bacterial attachment to these cells

Diagnosis: Purulent saliva sent for culture

a) Acute bacterial sialadenitis

• Uncommon disorder
• Usually involving the parotid gland as an ascending infection

Etiology:

• Strep pyogenes
• Staph aureus
• Strep viridans
• Haemophilus
• Debilitated/ dehydrated patients
• Sjogren syndrome
• Immune compromised patients

Clinical:

• Gland swelling
• Pain, fever, malaise
• Redness of overlying skin
• pus discharge
• Trismus/lockjaw
• Cervical lymphadenopathy

Management:

• Reverse the medical condition that may have contributed to formation
• Discontinue anti-sialogogues
• Warm compresses, maximize OH, give sialogogues (lemon drops)
• External salivary gland massage if tolerated
• Antibiotics:
  • 70% of organisms produce B-lactamase or penicillinas
  • Need B-lactamase inhibitor like Augmentin or Unasyn or 2nd gen cephalosporin
  • Can adding metronidazole or clindamycin to broaden coverage

• Failure to respond:
  • After 48 hours the patient should respond
  • Add 3rd gen cephalosporine
  • Add aminoglycoside
  • MRSA in nursing homes and nosocomial environments – vancomycin

• Surgery for acute parotitis:
  • Limited role for surgery
  • Discrete abscess – surgical drainage
  • 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

Complications:

• Hematogenous spread
• Direct extension- Abscess ruptures into external auditory canal and TMJ
• Fascial capsule around parotid deep surface is weak – it is adjacent to the loose areolar tissues of the lateral pharyngeal wall (Achilles ‘heel of parotid). Therefore extension of abscess- in parapharyngeal space may result in:
  • Airway obstruction
  • Mediastinitis
  • Internal jugular thrombosis
  • Carotid artery erosion
• Dysfunction of one or more branches of the facial nerve – rare
• Thrombophlebitis – retromandibular vein or facial veins – rare

b) Chronic bacterial sialadenitis

• Non specific inflammation
• Associated with long term diseases of the salivary gland
• Parotid more common

Clinical:

• Unilateral swelling
• Tenderness
• Inflamed duct orifice
• Purulent or salty discharge

Histology:

• Duct dilatation
• Hyperplasia of duct epithelium
• Periductal fibrosis
• Acinar atrophy
• Chronic inflammatory infiltrate

Sialography:

• Duct obstruction or stricture
• Destruction of glandular tissue
• Duct dilatation (sialectasia)

Management:

• Treat predisposing factor – calculus or stricture
• Initial mx should be conservative:
  • Sialagogues
  • Massage
  • Antibiotics for acute exacerbations.
• Should conservative measures fail, consider removing the gland

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Viral sialadenitis

Etiology:

• Droplet spread, incubation 2 – 3 weeks
• Mumps = acute, contagious infection mainly caused by paramyxovirus (RNA virus)
• Others causes of acute viral parotitis: coxsackie a & b, echo virus, cytomegalovirus and adenovirus

Clinical:

• Fever, malaise
• Painful swelling affecting the parotids (only in 70% of patients)

Physical exam:

• Glandular swelling (tense, firm) Parotid gland involved frequently, SMG & SLG
• Displace ispilateral pinna
• 75% cases involve bilateral parotids, may not begin bilaterally (within 1-5 days may
  become bilateral)….25% unilateral
• Low grade fever

Complications:

• Orchitis in 20% adult males (ensuing infertility is rare)
• Oophoritis – Ovary inflammation
• Pancreatitis
• Meningitis OR meneigoencephalitis
• Deafness

Diagnosis:

• IgM antibody titres
• ↑ Serum amylase
• ↑ Lipase
• Leukocytopenia, with relative lymphocytosis

Management:

• Antipyretics
• Analgesics
• Adequate hydration
• Isolate the patient 6 – 10 days after the onset of symptoms because the virus is in the saliva at this time

Prevention: MMR Vaccine: measles, rubella, mumps vaccine is administered in a single subcutaneous dose after 12 months of age. Booster at 4-6yr

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Post irradiation sialadenitis

• Common dose-related complication of radiotherapy
• Causes fibrous replacement of damaged acini & squamous metaplasia of ducts.
• Sialoliths = calcification within salivary duct, involves salivary gland also occur in 70 – 90% cases

Clinical:

• Pain & sudden enlargement of gland in relation to gustatory stimuli
• It is complicated by ascending infection & chronic sialadenitis

Histology:

• Acinar destruction and in case of sialolithiasis
• lamellated structure composed of CaPO4 & CaCO3

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Necrotizing sialometaplasia

Etiology: Ischaemia → infarction of salivary lobules

• Uncommon disorder, may be mistaken for malignancy
• Iatrogenic origin, possibly a reaction to ischemia or injury

Clinical: Deep crater-like mucosal ulcer, commonly on hard palate, persist for upto 8 weeks

Histology:

• Histologically may be mistaken for SCC
• Lobular necrosis of salivary glands
• Squamous metaplasia of ducts
• Mucous extravasation
• Inflammatory infiltrate surrounded by pseudoepitheliomatous hyperplasia

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