Facial swelling presents diagnostic challenges in pediatric patients due to its range of possible etiologies, which include infectious, inflammatory, traumatic, congenital, and neoplastic origins. Accurate diagnosis depends on clinical presentations, anatomical landmarks, and relevant imaging findings. Clinically, swelling may be acute with inflammation, non-progressive, slowly progressive, or rapidly progressive (1). Prompt identification of the underlying cause is essential for appropriate management.

Parotid swelling is most commonly the result of viral or bacterial infections. Parotitis typically presents with pain, glandular enlargement, swelling, xerostomia, and occasionally, fever (2). Trauma-induced parotitis is very rare, particularly without external bruising or hematoma, and typically results from high-energy mechanisms (3). Recognizing this atypical presentation is crucial for prompt and accurate management. Diagnosis of such cases in children with developmental disorders, such as autism spectrum disorder (ASD), is especially challenging due to altered pain responses, limited communication, increasing reliance on imaging and clinical suspicion.

The presented case report describes an atypical presentation of delayed-onset, trauma-induced parotitis with absence of external bruising in a child with ASD. This example emphasizes the importance of considering occult trauma in the differential diagnosis of facial swelling, particularly in pediatric patients with non-verbal conditions or communication impairments.

A 9-year-old boy with ASD presented at the emergency department with a 2-day history of progressive right-sided facial swelling without any external bruising following a minor fall while jumping on a couch (Figure 1). The fall was of low energy and was not associated with loss of consciousness, vomiting, seizures, or neck stiffness.

Over the subsequent 48 h, the swelling progressively increased and became painful, particularly during mastication. Discomfort during jaw movement resulted in difficulty with oral intake. There was no reported fever or malaise, no systemic signs of infection, nor dental pain, trismus, drooling, dysphagia, ear discharge, hearing changes, or facial weakness.

There was no history of similar episodes, recent travel, insect bites, or known allergies. Immunizations were up to date. There was no known immunodeficiency or family history of salivary gland disorders. The child's neurological status and behavior remained at baseline throughout the course of the illness.

Examination showed stable vitals and soft tissue swelling anterior to the right earlobe, consistent with the anatomical location of the parotid gland. The overlying skin was intact, non-erythematous, and not warm to the touch. No cervical lymphadenopathy was present. Ear, nose, and throat examinations were unremarkable. Systemic examinations were within normal limits, with no additional injuries identified.

Point-of-care ultrasound using a high-frequency linear (14–5 MHz) transducer was performed. Transverse and longitudinal sweeps were performed from the pre-auricular region across the masseter to fully assess both parotid glands. The Stensen duct was systematically interrogated, and gland dimensions were compared bilaterally. Color Doppler was applied to evaluate intraparenchymal vascularity and help distinguish inflammatory changes from abscesses or vascular lesions.

Ultrasound showed a normal, homogeneous left parotid gland (Figure 2a). The right parotid gland was enlarged with diffusely heterogeneous, predominantly hypoechoic parenchyma and scattered 1–3-mm anechoic foci, compatible with ductal ectasia and micro-collections (Figure 2b). The Stensen duct was patent, without intraductal echogenic focus or posterior acoustic shadowing; there was no discrete intraglandular hematoma or periparotid fluid collection. Findings are suggestive of edema and micro collection from blunt trauma. Color Doppler showed preserved, mildly increased intraparenchymal vascularity without a focal rim-enhancing collection (Figure 2c). This sonographic appearance favors an inflammatory parotitis pattern rather than the marked hyperemia commonly seen in bacterial parotitis. Also, the absence of systemic symptoms, lack of purulent collections, and CT confirmation of intact ductal and bony structures supported a diagnosis of traumatic parotid edema and inflammation rather than primary infection.

CT imaging revealed right parotid gland swelling with mild surrounding inflammation but no stones, abscesses, fractures, or injuries to adjacent structures, supporting a diagnosis of right-sided traumatic parotitis, as shown in Figure 3.

MRI, while superior for soft tissue detail, was avoided for this child with ASD due to the required duration and the potential need for anesthesia. CT was chosen for its speed and accessibility in trauma cases.

In the absence of systemic symptoms and based on imaging findings, conservative management with analgesics, hydration, a soft diet, and warm compresses was initiated. Antibiotics were withheld, given the absence of clinical or radiologic signs of infection, consistent with current recommendations. The patient's symptoms improved gradually over 5 days. At 2-week follow-up, the swelling had resolved completely, and the patient returned to baseline without complications.

Parotitis is commonly caused by infections (whether bacterial or viral) or of an autoimmune origin (4–6). Traumatic parotitis, especially in the absence of facial skeleton injury, bruising, or injury in the ductal structure, is rare inflammation of the parotid gland that can be due to direct or indirect injury (7). Few case reports have underscored the unusual presentation of traumatic parotitis and its complications including sialocele (3, 8, 9).

Mechanical trauma, including facial injury, endoscopic procedure complication, and oral trauma, can lead to parotid swelling by damaging the glandular tissue, leading to inflammation then duct obstruction or secondary infection (4, 6, 10). Rarely, trauma may exacerbate underlying sialolithiasis or may perform facial nerve compression leading to secondary gland dysfunction (10). Parotid swelling and parotid related complications may not appear until days or even months which leads to diagnostic confusion with neoplasms and infection (3, 11, 12). Delayed parotid swelling presentation, as reported in the literature, evolve gradually due to ductal obstruction, traumatic edema and venous congestion (6).

Traumatic parotitis symptoms usually overlap with other conditions which require a thorough deferential diagnosis to distinguish it from other parotid swelling and inflammatory causes. Diagnosis of such cases is challenging and depends on history taking (of mumps or viral infections), physical examination and imaging. Features like fever, malaise and purulent discharge usually suggest bacterial infections rather than traumatic parotitis (13). Imaging including ultrasound and computed tomography (CT) are usually used to exclude the presence of stones, abscess formation, ductal obstruction and neoplastic lesions (10, 13, 14). In some cases, laboratory investigations including IgE are used to exclude allergic parotitis and autoantibodies to exclude autoimmune parotitis (15, 16).

Injury assessment in children with ASD is complicated my multiple factors. Patients may present atypically, with communication difficulties that limit the patient in describing the symptoms or events, also they have sensory sensitivity and anxiety that make physical examination more difficult (17). Additionally, they have difficulties to tolerate long imaging procedures due to their anxiety and in ability to remain still unless sedation or special preparation is used (17). This underscores the importance of comprehensive history taking from parents or caregivers and maintaining a low threshold for diagnostic imaging in pediatric populations with non-verbal or sensory-sensitive conditions. Also, management plans should be tailored to be suitable for the patient's communication style, triggering behavior and sensory preferences (17).

The thick capsule and mandibular protection of the parotid gland render it resistant to blunt trauma; however, injury to the gland or duct can result in unilateral facial swelling with mild pain, due to duct obstruction or inflammation, which are best diagnosed using CT or sialography (8). The location of the parotid gland beneath parotid fascia, being embedded in fat and covered by platysma and other soft tissues provide a strong protection that even when substantial forces cause glandular damage there will be no visual skin changes (18).

Ultrasound is the first line modality to diagnose acute traumatic parotitis in pediatrics due to its safety (no exposure to radiation), gland morphology and vascularity accessibility and its ease in use in children (19). However, the clinical presentation of this case raised a concern that requires further anatomical investigation. Ultrasound has limited ability to visualize deep and retro-parotid spaces and thus limited ability to exclude occult hematomas and ductal injuries (20). Therefore, computed tomography (CT) was chosen as the appropriate modality to rapidly and accurately assess the extent of injury, rule out abscess formation and evaluate deep structure. It helps to give prompt and detailed assessment of the injuries however it involves significant radiation exposure, which is a concern in pediatrics, therefore it should be limited and minimized when possible (19, 21). MRI, although the superior in soft tissue contrast and visualization of nerves, requires sedation in young children especially those with ASD and are of less availability in acute settings, accordingly it wasn't used (19).

In this case, CT imaging excluded mandibular fracture and obstructive sialolithiasis and it revealed enlarged gland with mildly enlarged intraparotid lymph nodes. There was no fever, erythema, purulent discharge, leukocytosis or any systemic symptoms suggestive of bacterial parotitis. A conservative approach was recommended based on the absence of all clinical and imaging abnormalities that suggest abscess formation, sialolithiasis or ductal obstruction (8, 12, 22). Current pediatric literature supports that traumatic parotitis in children is self-limiting and responds well to supportive care including hydration, analgesics and glandular message (5). Antibiotic therapy is only warranted in cases with clinical evidence of infection (5, 22). Invasive diagnostic procedures were avoided, as there was no indication of salivary leakage or associated injuries, consistent with previous findings by Agrawal et al. (7) and similar reports described in the literature (12).

Trauma related symptoms may be underrecognized in ASD patients, therefore healthcare providers should be alert for the behavioral changes that could be a warning sign of pain or stress. Blunt parotid trauma in children, although rare, can often be managed conservatively once ductal injury is excluded, with excellent outcomes reported in the literature.

This case underscores the importance of considering trauma as an etiology for parotid swelling, even in the absence of external signs such as bruising or wounds. In children with ASD, atypical symptom expression may obscure the severity of underlying pathology; early imaging and vigilant clinical evaluation facilitated effective conservative management without complications. Ultimately, clinician awareness and diagnostic vigilance are key to avoiding unnecessary interventions and achieving favorable outcomes.