Subdural Empyema

Etiology

The etiology of subdural empyema can be multifactorial. However, some of the predisposing factors associated with the development of this condition include prior cranial surgery, head trauma with open skull fractures or penetrating injury, infected hematoma or subdural effusion, and improperly treated ear and sinus infections.[6][7] The literature reports that between 40% to 80% of patients with subdural empyema have otorhinologic infections, especially of the paranasal sinuses. Up to 20% of subdural empyemas occur following head trauma or cranial surgical procedures.[8]

The most frequently recovered microorganisms are anaerobes, aerobic streptococci, staphylococci, Haemophilus influenzae, Streptococcus pneumoniae, and other gram-negative bacilli. However, the most commonly reported microbial agents in cases of paranasal sinusitis-related subdural empyema are anaerobic and microaerophilic streptococci (Streptococcus milleri and Streptococcus anginosus).[9] Meanwhile, Staphylococcus aureus is the most common organism in cases arising from cranial trauma or surgical procedures. Coagulase-negative Staphylococci, anaerobes, and gram-negative organisms may also be found in these patients. Many infections are polymicrobial.[10][11]

Subdural empyema is usually a complication of purulent meningitis in young children.[1] In contrast, the condition is commonly secondary to direct extension from contiguous foci in older children.[12] Intracranial empyema can develop in children following COVID-19 infection and is often associated with cerebral sinus thromboses.[13] The pathophysiological mechanism in infants involves the infection of sterile, reactive subdural effusions from meningitis.[14] Subdural empyema due to bacterial meningitis is rare in adults.

Epidemiology

Intracranial subdural empyema usually affects children and young adults.[15] Male individuals are more commonly affected, with a male-to-female ratio of 3:1. Subdural empyemas can also develop in the spinal canal, though cases are rarely reported in the literature.[16] Intracranial subdural empyemas are much less common than brain abscesses.

Pathophysiology

Subdural empyema most often occurs from the direct extension of local infection, which can spread to the intracranial compartment due to the valveless diploic veins of Breschet. Consequently, blood may flow in either direction, causing intracranial bacterial infection to spread.[17] The lesions can also appear after a cranial surgical procedure due to the inoculation of microorganisms into the subdural space.

History and Physical

Subdural empyema initially presents with signs and symptoms of infection but may also be asymptomatic.[18] Manifestations may include fever, headache, nausea, vomiting, focal neurological deficits, seizures, and mental status changes. Fever and headache are usually present, and seizures occur in about half of patients; meningeal irritation signs may also be seen.

Most cases are gradually progressive; however, some patients can rapidly deteriorate, becoming drowsy, stuporous, and eventually comatose—or even die. Rapid progression may be due to increased intracranial pressure from the expanding pus collection. A recent head and neck infection, trauma, or surgery is often elicited.

Physical examination may show unstable vital signs, including fever, tachycardia, and respiratory compromise, which could all correlate with sepsis. The Cushing triad of hypertension, bradycardia, and bradypnea may be observed in severe cases. Other physical examination findings related to the neurological exam include meningismus, contralateral hemiplegia, cranial nerve palsies, anisocoria, and papilledema.[19]

A subdural empyema must be considered in a patient diagnosed with sinusitis or otitis who develops a fever, headache, and cranial pain. This disease should also be suspected in a patient who has recently undergone subdural hematoma drainage and presents with a fever, seizure, and new neurological deficits. Significant neurological deficits may occur due to localized brain edema and infarction associated with cortical thrombophlebitis.

Evaluation

History and physical examination should help tailor case evaluation and diagnosis. However, cranial imaging should be performed in all patients with suspected subdural empyema. The lesion appears as a hypodense area over a cerebral hemisphere or along the falx on a computed tomography scan. The collection margins are better delineated with the infusion of intravenous contrast dye. Depending on the extent and size of the subdural empyema, mass effects associated with the shifting of midline structures can also be seen. However, the diagnostic imaging study of choice for intracranial subdural empyema is magnetic resonance imaging (MRI) with intravenous gadolinium enhancement.

Contrast-enhanced MRI demonstrates sharp images of small collections and interhemispherically localized lesions. Subdural empyema is usually described in T1-weighted image findings as a "crescent-shaped" or "elliptical area" of hypointensity underneath the skull or adjacent to the falx cerebri. MRI diffusion-weighted imaging has proven to be more sensitive than routine MRI sequences and, therefore, should be performed.[20][21]

Laboratory workup can add evidence to the suspected diagnosis. The complete blood count often demonstrates leukocytosis, indicating an active infectious process, although this change may not always be found in immunosuppressed patients. Depending on the patient’s immune response, bacterial infections can cause a leftward shift with associated neutrophilia. Further laboratory testing, including serum inflammation markers like the erythrocyte sedimentation rate and C-reactive protein, could add evidence as these modalities are considered acute-phase reactants. Clinicians suspecting an infection may recommend blood culture samples to direct antibiotic therapy early in the disease course. However, the etiological agent is often difficult to identify due to the infection's encapsulated nature.[22][23] Spinal puncture does not help with diagnosis. The procedure can also be dangerous in patients with increased intracranial pressure and empyemas, which cause mass effects.

Treatment / Management

The treatment of cranial subdural empyema is multimodal, including medical and surgical interventions. Infectious disease and neurosurgery specialist involvement is indispensable. Monotherapy with antibiotics is rarely prescribed but may be considered in patients with mild presentations, no major neurological deficits, small pus collections on imaging, and documented early treatment response. However, such patients need close monitoring with serial clinical exams and neuroimaging studies. Longer antimicrobial therapy courses may be required. 

A prompt and accurate diagnosis, directly influenced by the clinician's suspicion based on the patient's history, physical examination, laboratory results, and imaging, often leads to a more favorable outcome. Treatment options, including multiple burr holes with drainage or a craniotomy for drainage and debridement, have been previously described in the literature. A craniotomy usually offers better results and fewer recurrences. Infants are treated with a burr hole, multiple subdural taps through the anterior fontanelle, or a craniotomy.

Preoperative imaging accurately localizes the pus collection, guiding the surgical approach. Once selected, multiple burr holes are made over the collection, allowing for incision of the dura mater, pus drainage, and irrigation of the cavity with saline solution. A large skin incision and wide craniotomy are required if a craniotomy is performed. Endoscopic evacuation of panhemispheric subdural empyemas may also be effective.[24]

A wide craniotomy is usually recommended for adequate exposure, thorough exploration, and complete evacuation of the subdural purulent collection. The dura is carefully opened to reveal the empyema, which typically presents as a collection of frank pus. A sample should be sent for both aerobic and anaerobic cultures.

The patient is started on antibiotics based on the results of Gram staining and the infection's pathogenesis until cultures are reported; broad-spectrum antibiotics should be initiated if Gram staining is negative or unavailable. Culture results guide the adjustment of antibiotic therapy. However, operative cultures can be negative, with no microorganisms reported in 7% to 53% of cases—often due to the frequent use of preoperative or preculture antimicrobial therapy.

Intravenous antibiotic therapy, coordinated by the infectious disease team for 3 to 6 weeks, is required. Longer treatment periods are warranted in patients with osteomyelitis. Infant subdural empyema is often secondary to meningitis, requiring 6 to 8 weeks of antibiotic administration.[25](B2)

Laboratory testing is critical for further monitoring and follow-up. The recommended imaging approaches include a repeat head computed tomography scan or brain MRI. Antiepileptic drugs should be given because of the high incidence of preoperative and postoperative seizures.

Differential Diagnosis

The differential diagnosis of intracranial subdural empyema includes conditions with features of infection and neurologic dysfunction, such as the following:

• Epidural abscess
• Brain abscess
• Brain tumor
• Leptomeningeal disease
• Subdural hematoma
• Meningitis
• Cerebritis
• Subdural hygroma

A thorough evaluation, including the appropriate use of imaging tests, can help guide treatment approaches.

Prognosis

The clinical outcome of subdural empyema depends on the preoperative level of consciousness, timing of intervention, and aggressiveness of the treatment. Awake and alert patients have a good prognosis in most cases, while stupor and those in a comatose state bear a high mortality risk. Older patients have the worst prognosis, and up to half of the patients have permanent residual neurological deficits. Further, late seizures may occur despite the use of antiepileptic medications, and those with brain herniation often have an unfavorable prognosis.

Complications

Subdural empyema's complications include seizures, cerebritis, cerebral abscess, cerebral edema, cortical venous thrombosis with cerebral venous infarction, cavernous sinus thrombosis, sepsis, septic shock, electrolyte imbalances, hydrocephalus, cranial osteomyelitis in adjacent cranial bones, osteomyelitis of the craniotomy bone flap, and residual neurological deficits.