Acute bacterial sinusitis (ABS) in childhood is common, complicating up to 7.5% of upper respiratory infections (1). While ABS leading to an intracranial abscess is rare, it has significant morbidity (1). ABS should be considered when children with upper respiratory infections show symptoms lasting longer than 10 days, a worsening course after initial improvement, or concurrent fever with purulent nasal discharge for at least 3 consecutive days (2). Allergic rhinitis is a further risk factor for the development of ABS (3). The development of a subdural empyema usually presents with persistent fever and worsening headache, followed by nausea and signs of meningeal irritation as intracranial pressure or inflammation increases (4,5). Seventy-eight percent of subdural empyema cases show altered mental status, focal neurologic deficits, seizures, or signs of meningeal irritation at the time of hospitalization (6). A written informed consent was obtained from the patient’s legal guardian for the publication of this report including all clinical images.

A 12-year-old girl was brought to the emergency department following a minor head injury with decreased consciousness for the preceding 90 minutes. She also had a 1-week history of fever and dry cough. Three hours prior to presentation, while she was walking to a school, she was noted to be unsteady on the feet and had 2 falls from her standing height resulting in hitting her head against the ground. Following the falls, she did not lose consciousness or experience any seizures and continued on her journey to the school. Shortly after arriving there, however, she was noted to be unarousable, and emergency medical services were called.

She had a background of right frontal lobe refractory epilepsy secondary to focal cortical dysplasia, autism spectrum disorder, and global developmental delay, as well as ongoing allergic rhinitis (not apparent at the presentation). At baseline, she was not verbally communicative. She had 1 or 2 self-aborting seizures a day lasting about 1 minute each. Long-term antiepileptic medications included phenytoin, clobazam, and lamotrigine. Her weight was 34.6 kg (10th percentile) and 149 cm (10th-25th percentile) according to the United States Centers for Disease Control and Prevention growth charts (7).

On arrival at the emergency department, her initial vital signs were as follows: blood pressure, 102/60 mmHg; heart rate, 115 beats/minute; respiratory rate, 30 breaths/minute; temperature, 38.2 °C; oxygen saturation, 100% on room air; and a Glasgow Coma Scale of 5 (eye-opening, 1; verbal response, 1; and motor response, 3). Her pupils were equal and reactive to light, with intact reflexes, but she was unable to move spontaneously. She had good respiratory effort. Despite there being a suspicion of ataxia or hemiparesis given the unsteady gait prior to arrival, we were unable to thoroughly assess this given her low Glasgow Coma Scale. There were no signs of meningeal irritation. There was a 1 cm-long bleeding laceration over the occiput, with otherwise normal physical examination findings.

Initial findings were as follows: white blood cells, 16.9 × 10⁹/L; C-reactive protein, 239 mg/L, alanine transaminase, 58 U/L; and aspartate transaminase, 67 U/L. Concentrations of electrolytes and urea were within the normal limits. There was a suggestion of end organ insult to the kidneys, with a creatinine concentration of 1.07 mg/dL (estimated glomerular filtration rate of 57 mL/minute/1.73 m²), which increased from a baseline value of 0.48 mg/dL (estimated glomerular filtration rate of 130 mL/minute/1.73 m²) taken 1 year prior to the presentation. Phenytoin concentration was 15 mg/L (therapeutic range, 10-20 mg/L). Toxicology screening turned out to be negative, such as paracetamol concentration and urine drug screen.

An initial head computed tomography (CT) showed findings in keeping with her underlying medical problems, with no signs of intracranial hemorrhage, skull fracture, or ischemic stroke (Fig. 1A). There was near-complete opacification of all paranasal sinuses and partial opacification of the left mastoid air cells. A chest radiograph, done in view of the fever with cough, was unremarkable. A respiratory multiplex polymerase chain reaction to screen for 18 common respiratory pathogens was negative.

The girl was started on intravenous (IV) ceftriaxone (2 g) for presumed sepsis with possible meningoencephalitis. IV lorazepam (0.1 mg/kg) was given in view of concerns for an ongoing nonconvulsive seizure. About 1 hour after her arrival, she regained full consciousness on the attempted insertion of a nasogastric tube. At this point, her presentation was thought to be reversible due to postictal confusion. Four hours later, however, her blood pressure dropped to 72/44 mmHg with a temperature of 39.7 °C, requiring boluses of 0.9% saline (total, 60 mL/kg) and subsequently an infusion of epinephrine (maximum of 0.1 μg/kg/minute). Antibiotics were escalated to piperacillin-tazobactam (90 mg/kg/dose) for septic shock of unclear source.

Blood cultures later grew Streptococcus anginosus, which was susceptible to penicillin, and antibiotics were changed back to ceftriaxone (2 g twice daily). On day 4, she became hemodynamically stable but was noted to have left eyelid swelling, prompting concern for ABS with orbital cellulitis. On day 5, a contrast-enhanced CT of the sinuses and orbits showed pansinusitis with blockage of bilateral frontal recesses, ostiomeatal units, spheno-ethmoidal recesses, olfactory clefts, and superior nasal meatuses, with no orbital involvement (Fig. 1B). At this point, the CT scan was thought not to show any obvious intracranial mass-like lesion.

On day 6, she underwent bilateral functional endoscopic sinus surgery. Intraoperatively, she had pansinusitis, and bacterial culture of the pus grew Staphylococcus lugdunensis. On the same day, a lumbar puncture was performed given the lack of a mass-like lesion on the CT scan, and showed a cerebrospinal fluid profile as follows: white cell counts; 63 cells/μL; glucose, 1.9 mmol/L; protein, 1.4 g/L; and lactate, 3.5 mmol/L, with a negative cerebrospinal fluid profile indicating aseptic meningitis. At this point, the sepsis was thought to be from ABS with central nervous system involvement. Clinically, she did not appear to have any focal neurological deficits or ataxia despite the limited neurological examination due to her altered mental status and baseline nonverbally communicative state. On day 8, brain magnetic resonance imaging (MRI) showed signs of subdural empyema (Fig. 2).

The girl remained lethargic and febrile. On day 18, she underwent craniotomy and evacuation of the subdural empyema for source control. Intraoperatively, she was found to have a subdural purulent collection with a thick capsule extending medially towards the falx cerebri, and anteriorly and inferiorly towards the skull base. Immediately after the surgery, her fever lysed and she regained her baseline mental status. On day 37, she was discharged after a period of uneventful recovery and rehabilitation. She completed 8 weeks of IV antibiotic therapy following the surgery and thereafter remained well with return to her baseline function. A follow-up MRI performed 4 weeks after the evacuation of the subdural empyema showed no recurrence of the collection.

ABS in childhood is common but rarely progresses to suppurative intracranial complications (1,4). Yet, it remains the most common cause of subdural empyema in children, where the infection spreads directly from contiguous sinuses or from drainage through emissary veins (8-10). Presentation of subdural empyema usually progresses from fever and headache, to vomiting, focal neurological deficits, seizures, or altered mental status (11).

A recent scoping review analyzing 33 studies describing 1,149 pediatric cases of intracranial complications of ABS, showed that most presented with nonspecific symptoms such as headache (56.9%), fever (47.5%), or nausea/vomiting (24.5%) (5). Prior case reports have mainly involved previously healthy children. Our case is unique in that the patient was a neurodivergent, nonverbally communicative child with limited ability to report her symptoms. Her diagnostic process was likely delayed due to the absence of vomiting and the presence of underlying neurological disorders and head injury, as well as due to the wide range of differential diagnoses.

The diagnosis was further delayed due to not identifying a subtle change on the contrast-enhanced CT on day 5, which was retrospectively thought to be an early lesion of subdural empyema (Fig. 1B). The lack of enhancement of the lesion may be explained by the fact that the lesion may have been at the phase of phlegmon, a non-cutaneous soft tissue inflammation, which had not yet developed into a wall-enhanced abscess (12). Gadolinium-enhanced MRI remains the gold standard in diagnosis of subdural empyema (13). Hence, where there is a change in mental status in the context of ABS, an MRI should be performed to rule out an intracranial abscess or empyema. This case also illustrates the importance of attentiveness to miscellaneous imaging findings, as the initial CT for trauma evaluation had already shown the opacification of the paranasal sinuses. In this context, such findings could have prompted earlier evaluation for intracranial complications of ABS.

The primary learning point is to have a low threshold to suspect ABS and be on the lookout for its suppurative intracranial complications when there are signs of neurological deterioration. This should be emphasized in neurodivergent patients because the diagnosis can be easily missed but poses serious outcomes.