We are uncertain of the status of this entity but have been shown putative cases of this disorder as described by Lyon and colleagues as “acute encephalopathy of obscure origin in children,” a febrile and sometimes fatal illness that could not be ascribed to direct infection of the nervous system. The term acute toxic encephalopathy, introduced by these authors still has some utility, but a careful search for better-characterized causes of febrile coma must be undertaken. During the height of a systemic bacterial or sometimes viral infection, the child sinks into coma, seizures are infrequent, the neck is supple, and the spinal fluid shows no changes or only a few cells. This is undoubtedly an illness of diverse causes, common among them being fluid overload and electrolyte imbalance, Reye syndrome (see Chap. 29) and, possibly most commonly, the immune condition of postinfectious encephalitis (see Chap. 35). Nonetheless, cases continue to be reported, such as those by Thi and colleagues, which can only be classified as a noninfectious bacterial encephalopathy or encephalitis. A relationship to the “septic encephalopathy” of adults, which has been emphasized by the group from London, Ontario, is possible but unproved. The acute necrotizing encephalopathy that has been reported, particularly in Asian children after influenza, probably belongs to this category and consists of a number of diseases as discussed by Mizuguchi and coworkers.
Subdural empyema is an intracranial (sometimes intraspinal) purulent process between the inner surface of the dura and the outer surface of the arachnoid that occurs mainly in children and is increasingly infrequent as various bacterial infections are treated earlier in their course. The infection usually originates in the frontal or ethmoid or, less often, the sphenoid sinuses and in the middle ear and mastoid cells. In infants and children, and infrequently in adults, there may be a spread from meningitis and the collection is then often sterile. The term subdural abscess, among others, had been applied to this condition but the proper name is empyema, indicating suppuration in a preformed space. Thrombosis of the underlying cortical veins and dural sinuses is a common accompaniment.
Usually the history includes reference to chronic sinusitis or mastoiditis with a recent flare-up causing local pain and increase in purulent nasal or aural discharge. In sinus cases, the pain is over the brow or between the eyes; it is associated with tenderness on pressure over these parts and sometimes with orbital swelling. General malaise, fever, and headache—at first localized, then severe and generalized and associated with vomiting are the first indications of intracranial spread. They are followed in a few days by drowsiness and increasing stupor, rapidly progressing to coma. At about the same time, focal neurologic signs appear, the most important of which are unilateral motor seizures, hemiplegia, hemianesthesia, aphasia, and paralysis of lateral conjugate gaze. Fever and leukocytosis are always present and the neck is usually stiff. Cases that follow surgery may be more indolent.
The usual CSF findings are an increased pressure, pleocytosis in the range of 50 to 1,000/mm3, a predominance of polymorphonuclear cells, elevated protein content (75 to 300 mg/dL), and normal glucose values. The spinal fluid is often sterile, but on occasion an organism is cultured. If the patient is stuporous or comatose, there is a risk associated with performing a lumbar puncture, and one should proceed first with imaging procedures. By imaging, one can see the ear or sinus lesions or bone erosion. The meninges around the empyema enhance and the collection of pus can be visualized more dependably with MRI. Empyema that follows meningitis in children tends to localize on the undersurface of the temporal lobe and may require coronal views to be well visualized.