Acute Bacterial Sialadenitis

Acute bacterial infection of a salivary gland, arising from retrograde ascent of oral flora through the duct into the gland parenchyma when salivary flow is reduced.

Pathogenesis

Saliva is protective: mechanical flushing, immunoglobulin A, lysozyme, lactoferrin, sialoperoxidase and a high fluid volume all inhibit bacterial ascent. Reduced flow removes this protection and permits retrograde migration of oral organisms.

The parotid is affected more often than the submandibular gland in non obstructive acute suppurative sialadenitis, which is the reverse of the pattern in sialolithiasis. Two factors explain this:

• Parotid saliva is serous and lacks the lysozyme rich mucinous content and higher immunoglobulin A concentration of submandibular saliva, so it has less intrinsic antibacterial activity.
• Stensen duct has a wider orifice and a more direct horizontal course.

Aetiology and risk factors

Reduced salivary flow, which is the common factor in almost every case:

• Dehydration, which is the dominant risk factor. Classically this occurs in the elderly postoperative patient who has been fasted, given anticholinergic premedication and opioids, and inadequately rehydrated, producing the entity historically known as surgical mumps, appearing 3 to 7 days after major surgery.
• Xerostomia inducing medications: anticholinergics, tricyclic antidepressants, antihistamines, antipsychotics, diuretics, beta blockers, opioids.
• Sjögren syndrome and post radiotherapy xerostomia.
• Obstruction from sialolithiasis or stricture.
• Debility, malnutrition, immunosuppression, diabetes, HIV, chemotherapy.
• Poor oral hygiene, which increases the oral bacterial load.
• Recent general anaesthesia and intubation.
• Advanced age.

Microbiology

• Staphylococcus aureus in 50 to 90 percent, including methicillin resistant strains in healthcare associated infection.
• Streptococcus viridans group, Streptococcus pneumoniae, Streptococcus pyogenes.
• Haemophilus influenzae.
• Anaerobes: Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus, which are present in a substantial proportion and which are frequently underappreciated, which is why anaerobic cover matters.
• Gram negative organisms including Escherichia coli, Klebsiella and Pseudomonas in hospitalised, immunocompromised and diabetic patients.

Neonatal suppurative parotitis, a distinct entity occurring in premature and dehydrated neonates, most often caused by Staphylococcus aureus, which presents with parotid swelling and purulent discharge from Stensen duct and which responds to intravenous antibiotics and rehydration.

• Rapid onset, over hours to a day or two, of painful unilateral gland swelling.
• Erythema, warmth and induration of the overlying skin.
• For the parotid: swelling that lifts the ear lobe outward and upward and obliterates the angle of the mandible, which distinguishes it from cervical lymphadenopathy which sits below and behind.
• For the submandibular gland: swelling in the submandibular triangle, best assessed bimanually.
• Trismus.
• Fever, rigors, malaise and anorexia.
• Purulent discharge from the duct orifice on gland massage, which is the diagnostic finding and which should be actively sought by milking the gland toward the orifice while observing the papilla.
• Foul taste.
• Reduced or absent saliva from the affected gland.
• Fluctuance where an abscess has formed, though a parotid abscess may not fluctuate because the dense parotid fascia contains it.

Red flags

• Systemic sepsis with hypotension and tachycardia.
• Facial nerve weakness, which is not a feature of simple inflammation and which indicates either an abscess with nerve compression or, more concerning, malignancy. Any patient with a parotid swelling and facial palsy requires imaging and tissue.
• Trismus with floor of mouth swelling and tongue elevation, indicating extension to the submandibular and sublingual spaces with Ludwig angina and airway risk.
• Extension into the parapharyngeal space, with medial displacement of the lateral pharyngeal wall.
• Crepitus or skin necrosis, indicating necrotising infection.
• Airway compromise.
• Immunocompromise or poorly controlled diabetes, which predict rapid deterioration.
• Bilateral swelling, which suggests mumps, HIV, Sjögren syndrome or sarcoidosis rather than bacterial infection.

• Clinical, based on acute painful gland swelling with purulent duct discharge in a patient with risk factors for reduced salivary flow.
• Culture and sensitivity of pus expressed from the duct orifice, obtained by milking the gland and collecting the discharge directly with a swab at the papilla. Request aerobic and anaerobic culture. This is the single most useful investigation and directs therapy.
• Full blood count showing neutrophilia, C reactive protein, urea and electrolytes to assess dehydration, glucose and HbA1c.
• Blood cultures where febrile or systemically unwell.
• Ultrasound, which is the first line imaging investigation: it demonstrates gland enlargement, heterogeneous hypoechoic parenchyma, increased vascularity, abscess formation as a hypoechoic collection with debris and posterior enhancement, ductal dilation and calculi. It also guides aspiration.
• Contrast enhanced computed tomography where abscess, deep space extension, airway compromise or malignancy is suspected, and where ultrasound is inconclusive. It defines the extent of a collection and its relationship to the parapharyngeal and masticator spaces.
• Magnetic resonance imaging for soft tissue detail and where malignancy is a consideration.
• Do not perform sialography during acute infection, since retrograde contrast injection can force organisms into the parenchyma and worsen the infection.
• Sialendoscopy is contraindicated during acute suppuration and is deferred until the episode has resolved.
• Mumps serology with immunoglobulin M, and buccal swab for mumps polymerase chain reaction, where the presentation is bilateral, the patient is unvaccinated, or there is a compatible epidemiological history.
• HIV testing, particularly in bilateral or recurrent disease.
• Anti Ro and anti La antibodies, and consideration of labial gland biopsy, where Sjögren syndrome is suspected.
• Fine needle aspiration cytology after resolution where a mass is suspected.

Differential diagnosis and the discriminating feature

• Mumps: bilateral in around 70 percent, non purulent, in an unvaccinated patient, with a prodrome and with orchitis, oophoritis, pancreatitis and meningitis as complications. Saliva is clear rather than purulent.
• HIV associated benign lymphoepithelial lesions: bilateral, cystic, painless, chronic.
• Sjögren syndrome: bilateral, recurrent, with dry eyes and dry mouth, and a raised risk of lymphoma.
• Sarcoidosis with Heerfordt syndrome, that is uveoparotid fever with parotid enlargement, uveitis, facial palsy and fever.
• IgG4 related disease with Küttner tumour of the submandibular gland, producing painless firm enlargement.
• Salivary gland neoplasm: a discrete mass rather than diffuse tender enlargement, with facial palsy in malignancy.
• Lymphadenitis, particularly intraparotid nodes, which are discrete and mobile.
• Odontogenic infection with masticator space involvement, producing trismus with normal salivary flow.
• Sialadenosis: bilateral, painless, non inflammatory, in diabetes, alcoholism, bulimia and malnutrition.
• Masseteric hypertrophy.

Rehydration, antibiotics, gland stimulation and drainage of any collection. The first three treat most cases; the fourth is required in 10 to 20 percent.

Rehydration and gland stimulation, which are as important as the antibiotics

• Aggressive rehydration, orally where possible and intravenously with 0.9 percent sodium chloride where oral intake is inadequate. Correcting the dehydration that permitted the infection is fundamental and is frequently underdone.
• Sialogogues: sour sweets, lemon juice, citrus drinks and chewing gum, used frequently through the day to stimulate flow and flush the duct.
• Gland massage from posterior to anterior toward the duct orifice, performed several times daily, which mechanically expresses pus and restores flow. Teach the patient or carer the technique.
• Warm compresses.
• Meticulous oral hygiene with regular brushing, and chlorhexidine mouthwash.
• Review and stop or substitute anticholinergic and other xerostomia inducing medications where clinically possible.
• Optimise glycaemic control.

Antibiotics

• Empirical cover must include Staphylococcus aureus and anaerobes.
• Oral therapy for mild disease in a well patient: co amoxiclav 625 mg three times daily for 7 to 10 days; or flucloxacillin 500 mg four times daily plus metronidazole 400 mg three times daily; or clindamycin 300 to 450 mg four times daily, which has excellent salivary gland penetration and covers both staphylococci and anaerobes and is a strong choice in penicillin allergy.
• Intravenous therapy for systemic illness, failure of oral therapy, immunocompromise, diabetes or suspected abscess: co amoxiclav 1.2 g every 8 hours; or flucloxacillin 2 g every 6 hours plus metronidazole 500 mg every 8 hours; or clindamycin 600 mg every 6 hours.
• Add vancomycin with a target trough of 15 to 20 mg/L, or teicoplanin, where methicillin resistant Staphylococcus aureus is prevalent or in healthcare associated infection.
• Add Gram negative cover with piperacillin and tazobactam 4.5 g every 6 to 8 hours in hospitalised, immunocompromised and severely unwell patients.
• Narrow therapy to the duct culture as soon as sensitivities are available.
• Convert to oral therapy when afebrile and improving, completing 10 to 14 days in total.

Analgesia

Paracetamol 1 g every 6 hours plus a nonsteroidal anti inflammatory drug where not contraindicated, with opioid titration for severe pain.

Abscess drainage

• Indicated for a demonstrated collection on ultrasound or computed tomography, and for failure to improve within 48 to 72 hours of adequate intravenous antibiotics.
• Ultrasound guided needle aspiration, which is minimally invasive, can be repeated, and is the reasonable first attempt for a small unilocular collection.
• Formal incision and drainage for larger or multiloculated collections.
• Parotid abscess drainage: a modified Blair or preauricular incision with a skin flap raised, then blunt dissection with artery forceps in a direction parallel to the branches of the facial nerve, spreading rather than cutting. Never make deep sharp incisions into the parotid. Use a facial nerve monitor where available. Place a drain.
• Submandibular abscess drainage: a transcervical incision two fingerbreadths below the mandible to protect the marginal mandibular nerve.
• Send pus for aerobic and anaerobic culture.
• Manage any extension into the parapharyngeal, submandibular or masticator spaces with formal deep neck drainage, and assess the airway.

Airway management

Floor of mouth involvement with tongue elevation, trismus and dysphagia indicates Ludwig angina with airway risk. Involve senior anaesthetic support early, plan for awake fibreoptic intubation or tracheostomy under local anaesthesia, and never induce anaesthesia in such a patient without a surgical airway plan and equipment prepared.

After resolution

• Identify and treat the underlying cause, which is essential to prevent recurrence.
• Ultrasound at 4 to 6 weeks to exclude a stone, a stricture and an underlying mass.
• Sialendoscopy where recurrent episodes occur, which identifies and treats stones, strictures and mucous plugs.
• Continue hydration, sialogogues and oral hygiene long term in patients with a persistent predisposing factor.
• Assess for Sjögren syndrome, HIV, diabetes and immunodeficiency in recurrent disease.
• Fine needle aspiration or imaging of any residual mass, since a neoplasm can present with secondary infection and can be masked by the acute episode.

Chronic recurrent sialadenitis

• Repeated episodes lead to acinar atrophy, ductal ectasia and fibrosis.
• Managed with hydration, sialogogues, massage, treatment of each acute episode, and sialendoscopy with ductal irrigation, steroid instillation and dilation of strictures, which is effective in a substantial proportion.
• Botulinum toxin injection into the gland to reduce secretion, and tympanic neurectomy or chorda tympani section to interrupt the parasympathetic supply, are options in refractory cases.
• Sialadenectomy is a last resort for a non functioning gland with intractable recurrent infection.

Juvenile recurrent parotitis

A distinct condition in children with recurrent episodes of unilateral or alternating parotid swelling, associated with sialectasis and immune dysregulation rather than bacterial infection primarily. It is managed conservatively with hydration, massage, sialogogues and antibiotics for acute episodes, and sialendoscopy with irrigation and steroid instillation is effective and reduces recurrence. Most cases resolve at puberty. Test for HIV and Sjögren syndrome in atypical or persistent cases.

Prevention

The highest yield intervention is preventing postoperative and hospital acquired parotitis through adequate hydration, oral hygiene, early oral intake, minimising anticholinergic medication and encouraging chewing in postoperative and elderly inpatients. These are simple nursing measures that are frequently neglected.