Pathogenesis Infection gains entry to the subdural space by direct extension through bone and dura or by spread from septic thrombosis of the venous sinuses, particularly the superior longitudinal sinus. Rarely, the subdural infection is the result of hematogenous spread from lung infection. Occasionally it extends from a brain abscess. It is currently predominantly the result of surgical procedures on the sinuses and cranium.
In cases originating after cranial surgery, staphylococcus is involved. Streptococci (nonhemolytic and viridans) are the most common organisms if the sinuses are the origin of infection, followed by facultative anaerobic streptococci (often Streptococcus milleri) or Bacteroides. Less often S. aureus, E. coli, Proteus, and Pseudomonas are causative. In about half the cases unrelated to surgery, no organisms can be cultured or seen on Gram stain.
Pathology A collection of subdural pus ranging from a few milliliters to 100 to 200 mL lies over the cerebral hemispheres. Pus may spread into the interhemispheric fissure or be confined there; occasionally it is found in the posterior fossa, covering the cerebellum. The arachnoid, when cleared of exudate, is cloudy, and thrombosis of meningeal veins may be seen. The underlying cerebral hemisphere is compressed, and in fatal cases there is often an ipsilateral temporal lobe herniation. Microscopic examination discloses various degrees of organization of the exudate on the inner surface of the dura and infiltration of the underlying arachnoid with small numbers of neutrophilic leukocytes, lymphocytes, and mononuclear cells. Thrombi in cerebral veins seem to begin on the sides of the veins nearest the subdural exudate. The superficial layers of the cerebral cortex undergo ischemic necrosis, which probably accounts for focal seizures and other signs of disordered cerebral function (Kubik and Adams).
Several conditions must be distinguished clinically from subdural empyema: a treated subacute bacterial meningitis, cerebral thrombophlebitis, brain abscess (see in the following text), herpes simplex encephalitis (see Chap. 32), acute disseminated encephalomyelitis and necrotizing hemorrhagic leukoencephalitis (see Chap. 35), and septic embolism because of bacterial endocarditis (see further on in this chapter).
Treatment Most subdural empyemas, by the time they are recognized clinically, require drainage through multiple burr holes, or through a craniotomy in cases with an interhemispheric, subtemporal, or posterior fossa location. The surgical procedure should be coupled with appropriate antibiotic therapy, generally a third- generation cephalosporin and metronidazole. Bacteriologic findings or an unusual presumed source may dictate a change to different drugs, particularly to later-generation cephalosporins. Without such antimicrobial therapy and surgery, some patients will die, usually within 7 to 14 days. On the other hand, patients who are treated promptly may make a surprisingly good recovery, including full or partial resolution of their focal neurologic deficits.
As with certain small brain abscesses, small subdural collections of pus that are recognized by CT or MRI before stupor and coma have supervened may respond to treatment with antibiotics alone. The resolution (or lack thereof) of the empyema can be readily followed by repeated imaging of the brain (Leys et al).