Subdural Empyema

Etiology

The etiology of subdural empyema can be multifactorial; however, some of the predisposing factors associated with the development of subdural empyema include prior cranial surgery, head trauma with open skull fractures, or penetrating injury, infected hematoma or subdural effusion, and not properly treated ear and sinus infections. Of the reported literature, up to 40 to 80% of patients with subdural empyema have otorhinologic infections, especially paranasal sinuses.[2] Up to 20% of the subdural empyemas occur following head trauma or cranial surgical procedures.[5]

The most common microorganisms are anaerobes, aerobic Streptococci, Staphylococci, Haemophilus influenzae, Streptococcus pneumoniae, and other gram-negative bacilli.[3] However, in cases of subdural empyema secondary to paranasal sinusitis, the most common microorganisms reported have been anaerobic and microaerophilic streptococci (Streptococcus milleri and Streptococcus anginosus).[3][6] In those cases secondary to cranial trauma or surgical procedures, the most common organism is Staphylococcus aureus.[4] Coagulase-negative Staphylococci, anaerobes, Gram-negative organisms can also be found in those cases of trauma or surgical procedures.[1] Many infections are polymicrobial.[6][7][8] Subdural empyema is usually a complication of purulent meningitis in infants, whereas, in older children, it is commonly secondary to direct extension from contiguous foci.[3][6][9][10] The mechanism of the development in infants is through infection of sterile, reactive subdural effusions secondary to meningitis.[10] In adults, subdural empyema secondary to bacterial meningitis is rare.[9]

Epidemiology

Intracranial subdural empyema usually affects children and young adults.[1] Males are more commonly affected, with a male to female ratio of 3:1.[1][6] Subdural empyemas can also develop in the spinal canal but are rarely reported in the literature.[4][1][11] Intracranial subdural empyemas are much less common than brain abscesses.[2]

Pathophysiology

Subdural empyema most often occurs due to the direct extension of local infection. The infection can spread to the intracranial compartment due to the valveless diploic veins of Breschet. As a result, blood may flow in either direction, causing the spread of bacterial infection intracranially.[12][2][9] They can also occur after cranial surgical procedures secondary to the inoculation of microorganisms into the subdural space, further developing into a subdural empyema.

History and Physical

Subdural empyema usually presents with signs and symptoms of infection; however, it can also be asymptomatic.[13] Some of the symptoms that can be seen 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 the patients.[6][2][10][9] Signs of meningeal irritation can also be seen.

Physical examination can show unstable vital signs, including fever, tachycardia, and respiratory compromise, which could all correlate with sepsis. Presentation in most cases is gradually progressive, and if untreated, symptoms may worsen. Some patients can become critically ill quickly, becoming drowsy, stuporous, and eventually comatose or even die.[3] This can be a result of increased intracranial pressure caused by the subdural empyema, which, in turn, can result in Cushing’s triad of hypertension, bradycardia, and bradypnea.

Other physical examination findings related to the neurological exam include meningismus, contralateral hemiplegia, and cranial nerve palsies, anisocoria, and papilledema.[14] A subdural empyema must be considered in a patient diagnosed with sinusitis or otitis who develops a fever, headache, and cranial pain. It should also be considered in a patient who underwent drainage of a subdural hematoma who presents with a fever, seizure, and new neurological deficits. Significant neurological deficits may occur and are caused by localized brain edema and infarction associated with cortical thrombophlebitis.[6][8]

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.[3][14] Subdural empyema appears as a hypodense area over the cerebral hemisphere or along the falx on a computed tomography scan. The collection margins are better delineated with the infusion of intravenous contrast dye.[3] Depending on the extent and size of the subdural empyema, associated mass effect with the shifting of midline structures can also be seen. The diagnostic imaging study of choice for intracranial subdural empyema is magnetic resonance imaging (MRI) with intravenous gadolinium enhancement. MRI shows better small collections and those that are localized interhemispheric. Imaging findings are usually described as a crescent-shaped or elliptical area of hypointensity on T1-weighted images underneath the skull or adjacent to the falx cerebri.[6] MRI diffusion-weighted imaging sequences have proved to be more sensitive than routine MRI sequences and, therefore, should be performed.[15][16][17]

Laboratory workup can add evidence to the suspected diagnosis. Leukocytosis can be seen, indicating an active process of infection. Immunocompromised or immunosuppressed patients will not always present with elevated white blood cells on complete blood count. Depending on the patient’s immune response, bacterial infections can cause a leftward shift with associated neutrophilia. Further laboratory workup, including serum inflammation markers such as erythrocyte sedimentation rate and C-reactive protein, could add evidence as these are considered acute phase reactants. In cases of infections, some clinicians may recommend blood culture samples to try direct antibiotic therapy early in the disease course; however, in the case of subdural empyema, these rarely identify an organism due to the capsulated nature of the infection.[17][18] 

Spinal puncture is not indicated for the diagnosis and can be dangerous in those patients with increased intracranial pressure and empyemas, causing mass effect.[4][2][6][10]

Treatment / Management

The treatment of cranial subdural empyema is multimodal, including both medical and surgical treatment. Infectious disease service and neurosurgery service are indispensable. The use of antibiotic therapy alone is rare; however, it can be used if the patient is essentially doing well, has no major neurological deficit, the collection is small, and an early response is documented.[8] However, such patients need close monitoring with serial clinical exams and neuroimaging studies. Longer courses of antimicrobial therapy may be required. (B2)

A prompt and accurate diagnosis will result in a more favorable clinical outcome, and this directly depends on the level of suspicion the clinician has as a result of the patient’s history, physical examination, laboratory workup, and imaging findings. Treatment options, including multiple burr holes or a craniotomy for drainage and debridement, have been previously described in the literature. A craniotomy usually offers better results and fewer recurrences.[7] Infants are treated with a burr hole, multiple subdural taps through the anterior fontanelle, or a craniotomy.[9][10] Preoperative imaging will help in accurately localizing the site of pus collection, which will direct where the surgery is to be performed.[3] Once the surgical area is chosen, multiple burr holes can be performed over the collection, and after the dura mater is incised, the pus is drained, and the cavity irrigated with saline solution. When a craniotomy is chosen, a large skin incision followed by a wide craniotomy is performed. A wide craniotomy is usually recommended as it allows for adequate exposure, exploration, and possibly more complete evacuation of the subdural purulent collection.[3] The dura is opened carefully, and the subdural empyema will be encountered as a collection of frank pus. A sample should be sent to the laboratory for both aerobic and anaerobic cultures.[3] The patient is started on antibiotics based on the results of the Gram staining and the pathogenesis of the infection until cultures are reported. If Gram staining is negative or unavailable, the patient should be started in broad-spectrum antibiotics. Cultured microorganisms will help adjust the desired antibiotic therapy. Unfortunately, operative culture results can be negative without any reported microorganisms in up to 7% to 53% of patients.[6] This can be accounted for due to the frequent use of preculture/preoperative antimicrobial therapy.[6](B2)

Intravenous antibiotic therapy, coordinated by the infectious disease team for 3 to 6 weeks, is required. Longer periods of therapy are required for those patients with osteomyelitis. In infants, subdural empyema is often secondary to meningitis, and antibiotic therapy is required for 6 to 8 weeks.[19](B2)

Further monitoring and follow-up can be done with laboratory workup. Imaging can be done with a repeat head computed tomography scan or brain MRI. Antiepileptic drugs should be given in view of the high incidence of preoperative and postoperative seizures.[7](B2)

Differential Diagnosis

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

Prognosis

The outcome is dependent on the preoperative level of consciousness, the timing of intervention, and the aggressiveness of the treatment. Awake and alert patients have a good prognosis in the majority of the cases. Stuporous and comatose patients have high mortality. Older age patients have the worst prognosis.[8] Up to half of the patients have permanent residual neurological deficits.[7] Late seizures may occur despite the use of antiepileptic medications.[1][7] An unfavorable prognosis can be seen in cases of brain herniation.

Complications

Complications of subdural empyema 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.[3][14][6]