Fulminant Bacterial Meningitis

FIGURE 4.1 CT scans shows early hydrocephalus (A) MRI shows dramatic meningeal enhancement. (B) Also, evidence of restricted diffusion in bilateral frontal temporal cortex indicative of additional laminar cortical necrosis due to infarction (C). MRA showed no evidence of arterial occlusions.

Cerebral edema is mostly cytotoxic and can have a particularly rapid onset with subsequent loss of some brainstem reflexes. Immediate aggressive use of osmotic diuretics and high dose of intravenous corticosteroids may turn the tide, but many patients may progress further to loss of all brainstem reflexes.

Several causes of deterioration are untreatable. The development of ischemic lesions—as shown in our case—may be due to vasospasm, vasculitis, or vasculopathy. Cortical infarctions are common and widespread and rarely lead to swelling or mass effect. These abnormalities on CT scan are often mislabeled as “cerebritis.” Vasculitis (or thrombotic vasculopathy) may lead to ischemia.

Brain injury can be rapid and permanent after an overwhelming infection. There is evidence that the brain may be an innocent bystander with leukocytes, macrophages, and microglia acting against invading bacteria, but at the same time releasing neurotoxic free radicals, proteases, cytokines, and other substances that result in neuronal cell death.

In our patient hydrocephalus was considered symptomatic despite the other areas of ischemic injury. A ventriculostomy was placed, and improvement of level of arousal occurred up to the point that extubation could be pursued. Nonetheless the patient remained severely impaired, uncommunicative, in need of gastrostomy and full nursing care. She died of a cardiac arrhythmia after the family had requested a do-not-resuscitate order.

Fulminant bacterial meningitis may be hard to treat effectively, and secondary manifestations (cerebral infarcts and hydrocephalus) may make recovery much less likely. Mortality in bacterial meningitis in the acute phase may be due to sepsis or multi-organ failure, but we suspect palliative care may be the most common reason of death in patients who remain comatose.

KEY POINTS TO REMEMBER IN FULMINANT BACTERIAL MENINGITIS

Treat aggressively with corticosteroids and broad spectrum antibiotics as early as possible.
MR imaging may explain neurologic condition.
Patients may not improve due to cerebral infarcts or severe meningeal inflammation causing hydrocephalus.
Cerebral edema may require osmotic diuretics and additional high dose corticosteroids.

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