Acute sialadenitis is acute inflammation of salivary glands. It may have bacterial (most commonly S. aureus) or viral (mumps — paramyxovirus) etiology. Bacterial sialadenitis usually develops in the setting of dehydration, poor oral hygiene, obstruction (sialolithiasis), or immunosuppression and is usually unilateral. Viral sialadenitis (mumps) is characterized by bilateral parotid enlargement. The parotid gland is the most commonly affected gland. Clinically, it presents with pain, swelling, redness, fever, and tenderness on palpation. Purulent discharge from the duct orifice supports bacterial infection. If untreated, it may progress to abscess formation. Dehydrated elderly patients, postoperative patients, and immunosuppressed individuals are at risk. Recurrent sialadenitis may be associated with juvenile recurrent parotitis or IgG4-related disease.
Age Range
20-70
Peak Age
40
Gender
Equal
Prevalence
Common
The imaging findings of acute sialadenitis are based on the inflammatory cascade and tissue changes. Bacterial infection enters retrograde through the duct orifice; decreased salivary flow (dehydration, obstruction) facilitates bacterial colonization. Inflammatory mediators create increased vascular permeability, edema, and neutrophil infiltration — these changes are reflected on imaging as gland enlargement, diffuse enhancement increase, and periglandular fat infiltration. Edema causes T2 hyperintensity. Duct wall inflammation manifests with duct wall thickening and luminal narrowing. Untreated bacterial sialadenitis progresses to microabscess formation; coalescing microabscesses form macroabscesses — seen as hypodense/hypointense collections with rim enhancement. Viral sialadenitis (mumps) shows bilateral parotid involvement; viral replication occurs in acinar cells and creates interstitial edema and lymphocytic infiltration.
Acute sialadenitis triad: diffusely enlarged gland, increased enhancement, and periglandular fat stranding. These combined findings strongly support inflammatory etiology and distinguish from tumor.
On B-mode ultrasonography, acute sialadenitis appears as diffuse gland enlargement with homogeneous or heterogeneous hypoechoic parenchyma. The heterogeneous transformation of normal gland structure reflects inflammatory edema and cellular infiltration. Intraglandular lymph nodes may appear reactively enlarged. The duct wall may be thickened and duct lumen dilated. In abscess formation, focal anechoic or hypoechoic collections with internal debris are observed. Periglandular fat tissue shows echogenic infiltration. Increased vascularity (hyperemia) on Doppler supports inflammatory activity. US is the preferred modality for initial evaluation and follow-up.
Report Sentence
The parotid gland is diffusely enlarged with heterogeneous hypoechoic parenchyma; increased vascularity is present on Doppler examination, consistent with acute sialadenitis.
On contrast-enhanced CT, acute sialadenitis is characterized by diffuse gland enlargement, increased and heterogeneous enhancement. Periglandular fat stranding demonstrates spread of inflammation to surrounding tissues. Platysma muscle thickening and subcutaneous edema are additional findings. Ductal dilation suggests the presence of obstruction — stone should be investigated. In abscess formation, a hypodense collection with peripheral rim enhancement is observed. Multiple small low-density foci within the gland may represent microabscesses. Cervical lymphadenopathy may develop reactively. CT is superior to MRI and US for evaluating complications (abscess, cellulitis, mediastinal extension).
Report Sentence
On contrast-enhanced CT, the parotid/submandibular gland is diffusely enlarged with increased enhancement; periglandular fat stranding and subcutaneous edema are present, consistent with acute sialadenitis.
On T2-weighted sequences, acute sialadenitis appears as diffuse hyperintensity (edema) and enlargement of the gland parenchyma. T2 hyperintensity in periglandular soft tissues reflects edema and inflammation. The abscess cavity shows markedly hyperintense T2 signal; the abscess wall may be identified as a hypointense rim on T2. Ductal dilation appears as a tubular structure filled with T2 hyperintense fluid. On T1, gland parenchyma is isointense to mildly hypointense, with diffuse enhancement increase on post-contrast series. On DWI, marked diffusion restriction (low ADC) in the abscess cavity reflects the high viscosity and cellularity of purulent content.
Report Sentence
On T2-weighted sequences, the parotid/submandibular gland demonstrates diffuse hyperintense signal with gland enlargement; edema is observed in periglandular soft tissues, consistent with acute sialadenitis.
On Doppler ultrasonography, acute sialadenitis is characterized by diffusely increased vascularity (hyperemia). Color Doppler shows widespread flow signals within gland parenchyma — while Doppler signal is minimal in normal parotid parenchyma, it shows marked increase in acute inflammation. Power Doppler is more sensitive and can also demonstrate low-flow inflammatory neovascularization. In abscess formation, peripheral hyperemia is seen around the abscess wall while no Doppler signal is present within the abscess cavity (avascular). Low resistive index on spectral Doppler reflects inflammatory vasodilation. Decreased vascularity on Doppler during treatment response correlates with clinical improvement.
Report Sentence
On Doppler examination, diffusely increased vascularity (hyperemia) is observed in the parotid/submandibular gland parenchyma; this finding is consistent with an active inflammatory process.
On DWI, the abscess cavity demonstrates marked diffusion restriction — hyperintense on DWI, hypointense signal on ADC maps. This finding is critical for distinguishing abscess from necrotic tumor and simple serous fluid collection. Simple fluid collections do not show diffusion restriction (high ADC). Diffusion restriction in necrotic tumors is variable. Purulent material in the abscess cavity contains dense neutrophils, bacteria, protein, and cellular debris — this structural complexity strongly restricts water diffusion. ADC values are generally <0.7 × 10⁻³ mm²/s.
Report Sentence
On DWI, the collection within the salivary gland demonstrates marked diffusion restriction (ADC: [value] × 10⁻³ mm²/s), consistent with abscess formation.
Criteria
S. aureus or other bacterial agent. Unilateral. Purulent discharge from duct orifice.
Distinct Features
Unilateral, purulent drainage, high risk of abscess formation, antibiotic treatment, obstruction should be investigated.
Criteria
Paramyxovirus infection. Bilateral parotid involvement. Mostly in childhood.
Distinct Features
Bilateral parotid enlargement, no purulent drainage, abscess rare, self-resolving, preventable by vaccination.
Criteria
Intraglandular or periglandular abscess formation. Complication of untreated bacterial sialadenitis.
Distinct Features
Rim enhancement, DWI diffusion restriction, fluctuant mass, requires surgical drainage, risk of progression to mediastinitis.
Distinguishing Feature
Sialolithiasis shows hyperdense calculus on CT, echogenic focus + posterior shadow on US. Acute sialadenitis may be secondary to obstructive stone — stone should be investigated.
Distinguishing Feature
Lymphoma is a solid homogeneous mass, very low ADC, periglandular fat stranding generally absent, FDG avid, may be bilateral but inflammatory signs (fever, tenderness, purulent discharge) are absent.
Distinguishing Feature
IgG4-related sialadenitis is bilateral, chronic course, homogeneous gland enlargement, T2 hypointensity (fibrosis), fever/tenderness generally absent, serum IgG4 elevated, lacrimal gland involvement may be present.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
Bakteriyel sialadenitis: antibiyotik (amoksisilin-klavulanat veya klindamisin), hidrasyon, sıcak kompres, sialogog stimülasyon, masaj. Apse geliştiğinde cerrahi veya US-kılavuzlu drenaj. Obstrüktif taş araştırılmalı ve tedavi edilmeli. Viral sialadenitis: semptomatik tedavi, kendiliğinden düzelir.Acute sialadenitis is a condition requiring urgent medical treatment. In bacterial form, empirical antibiotic therapy should be started immediately — broad-spectrum antibiotics covering S. aureus (amoxicillin-clavulanate or clindamycin) are preferred. Hydration, warm compress application, and sialagogue stimulation (lemon juice) increase salivary flow, alleviating obstruction. In abscess formation, surgical incision-drainage or US/CT-guided percutaneous drainage is mandatory. Untreated abscess can spread to the parapharyngeal space and mediastinum (Ludwig's angina, mediastinitis — life-threatening complications). In the presence of obstructive stone, treatment of the stone (sialendoscopy, surgery) prevents recurrence.
Clinical correlation is required.