Parotitis

Aetiology

Parotitis (inflammation/swelling of the parotid gland) has a wide range of causes:

• Acute infective — suppurative (aerobes: S. aureus, H. influenzae, Streptococcus spp.; anaerobes: Fusobacterium, Bacteroides, Peptostreptococcus; often polymicrobial), or viral (mumps/paramyxovirus, EBV, influenza, parainfluenza, Coxsackievirus, CMV, HIV).
• Chronic infective — TB, Actinomyces, syphilis.
• Obstructive/chronic — duct/gland scarring; sialolithiasis; benign (pleomorphic adenoma, Warthin tumour) or malignant (mucoepidermoid carcinoma, adenoid cystic carcinoma, SCC) neoplasm; radiation sialadenitis; cystic fibrosis.
• Chronic autoimmune — Sjögren syndrome; SLE; sarcoidosis (uveoparotid fever); granulomatosis with polyangiitis; rheumatoid arthritis; IgG4-related disease.
• Drug-induced — established (clozapine, phenylbutazone) or via reduced salivary secretion (anticholinergics, antiparkinsonian medications, antihistamines, sulfamethoxazole).
• Metabolic (sialadenosis) — diabetes; eating disorders; alcohol use disorder.

Acute suppurative parotitis

Demographics: classically older patients; risk factors include recent major surgery, diabetes, immunosuppression, hypothyroidism, and malnourishment.

History: rapid facial and neck swelling with increasingly severe pain, developing over hours to days — usually preceded by dehydration and/or strenuous activity reducing salivary flow, allowing retrograde bacterial ascension up Stenson’s duct. Decreased oral intake, dysphagia, trismus, and reduced neck range of motion reflect spread of inflammation to adjacent muscles. Fever strongly suggests an infective cause.

Examination: asymmetrical, diffuse facial swelling with severe tenderness, warmth, induration, and erythema, often crossing the angle of the mandible. The parotid papilla (Stenson’s duct opening, on the buccal mucosa opposite the second maxillary molar) may be oedematous and erythematous. Assess salivary flow by pressing posterior-to-anterior across the parotid while observing the papilla — expressed pus indicates bacterial infection and should be cultured. Always assess trismus (<3 finger-widths between incisors) and formally examine facial nerve (CN VII) function — a new branch palsy needs urgent ENT referral to exclude malignancy (rare cases of benign infective parotitis/abscess causing CN VII palsy exist, but malignancy must be excluded first). Distinguish diffuse parotid swelling from a focal, discrete mass (possible lymph node, abscess, or neoplasm) — the latter warrants imaging.

Investigations: baseline/progress bloods (FBC, U&E/creatinine, CRP). Culture any purulent duct discharge — S. aureus causes ~80% of acute suppurative parotitis, but community MRSA rates are rising. If systemic causes are suspected, targeted serology (ENA/ANA for Sjögren’s, anti- dsDNA for SLE, ACE for sarcoidosis, ANCA for GPA, RF/anti-CCP for RA, IgG4, HbA1c, viral titres, syphilis serology).

Imaging: not needed for straightforward acute parotitis, but useful to exclude complications or obstruction/neoplasm. Ultrasound is first-line to differentiate a focal mass and identify sialoliths ≥3mm (sensitivity 94.7%, specificity 97.4%). CT is 96% sensitive/100% specific for sialoliths and best for excluding infective complications (parotid/parapharyngeal collections) and surgical planning. MRI has limited acute-phase use but is best for differentiating chronic parotitis from benign/malignant neoplasia.

Management: empirical anti-staphylococcal antibiotics — flucloxacillin 500mg four times daily for 10 days, or clindamycin/ trimethoprim-sulfamethoxazole if MRSA risk or penicillin hypersensitivity. Reassess during treatment; minimal response by 48–72 hours needs urgent hospital referral ± imaging. Promote salivary flow: early rehydration, sialagogues (ascorbic acid, lemon juice, mints), hot compresses, regular parotid massage. A short oral steroid course (e.g. prednisolone 25mg for 3 days) can help trismus alongside simple analgesia, weighed against individual risk.

Red flags warranting ED/specialist referral: severe limitation of neck movement, dysphagia, or severe trismus limiting oral intake; systemically unwell (fever >38°C, tachycardia, hypotension, altered mental state, malaise); moderate-severe dehydration; a fluctuant, localised/discrete mass over the parotid; new facial nerve branch palsy; a fistula/sinus to overlying skin; imaging showing a collection/abscess, secondary collection, septic thrombophlebitis (Lemierre syndrome), or an associated neoplasm. Have a low threshold to refer socially isolated or vulnerable patients (older, rural/remote).

Viral parotitis (including mumps)

Suspect mumps first in bilateral parotid swelling with fever. 40–50% of mumps patients have respiratory symptoms; 20–30% of post-pubertal males develop orchitis; 10% develop aseptic meningitis. Despite vaccination, Australian outbreaks continue, disproportionately affecting Aboriginal and Torres Strait Islander communities (60.5% of cases, 2016–2019). Mumps is a nationally notifiable condition — report to the state health authority when diagnosed. Confirm with mumps IgM serology and/or buccal PCR.

Demographics: children <15 years; those in close quarters (e.g. sports teams).

History: 2–3 week incubation; prodrome of fever, malaise, headache, myalgia, arthralgia, anorexia; salivary gland swelling starting unilateral then becoming bilateral, usually lasting 1–5 days.

Examination: skin overlying the gland is not red or warm (redness/warmth suggests bacterial cause).

Management: self-resolving, managed expectantly — continue salivary-flow techniques and adequate hydration. No specific antiviral treatment for mumps; self-isolate from work/school for 5 days after onset. Supportive: pain relief, artificial saliva, sialagogues (e.g. lemon).

Complications of mumps: orchitis (20–30% of post-pubertal males); oophoritis (~5% of females); also mastitis, pancreatitis, aseptic meningitis, sensorineural hearing loss, haemolytic anaemia, thrombocytopenia. Patients are contagious for up to 9 days after onset of parotid swelling.

Referral to ENT (outpatient)

Two or more episodes of parotitis on the same side; imaging-confirmed sialolithiasis with ≥1 episode of parotitis on the affected side; bilateral or recurrent parotitis without a clear infective/obstructive cause needing further work-up. Urgent outpatient referral for any parotid mass, lesion, or neoplasm found incidentally on imaging.

Postoperative parotidectomy — common presentations in primary care

Up to 4 in 5 parotid neoplasms are benign (pleomorphic adenoma and Warthin tumour most common); malignancy comprises ~20% of parotid tumours. GPs commonly see patients after parotidectomy with:

• Facial muscle weakness (temporary in up to 42%, resolving in 38% by 1 month and 78% by 3 months; permanent/synkinesis <1%) — manage conservatively with reassurance and monitoring; nocturnal eye protection and lubricating drops if eye closure is affected (corneal injury risk); progression of weakness warrants urgent surgical referral.
• Altered sensation in the great auricular nerve distribution (common, ~34%) — conservative management; increasing severity warrants urgent surgical referral.
• Scarring and facial contour asymmetry — common to some degree in all patients, usually improves over time; reassurance, scar massage; surgical referral for severe keloid/hypertrophic scarring (~4%).
• Frey syndrome (gustatory facial flushing/sweating with meals) — common (up to 60%), severe in up to 15%; re-refer to the treating surgeon for consideration of botulinum toxin injection.
• Sialocele (a fluid collection from a salivary leak, presenting as fluctuant swelling near the wound, often after eating) and first-bite syndrome (severe pain with the first bite of each meal, from parasympathetic denervation supersensitivity, most associated with deep-lobe/parapharyngeal surgery) are other recognised post-parotidectomy phenomena — re-refer to the surgical team for ambiguous, unresolving, or worsening presentations rather than managing empirically in general practice.