Subcutaneous unfractionated or low molecular weight heparin

worse overall outcome.21 Patients with brain injury may become febrile from a host of different causes, most commonly including pneumonia, urinary tract infection, medications, and DVT, and these entities may contribute to worse outcomes for non-neurological reasons. The term "neurogenic fever'' is reserved for situations in which patients with a primary cerebral insult experiences fever, but no secondary causes are found. The severity and duration of the fever appear to directly correlate with the degree of brain injury, as well as with the presence of intracerebral hemorrhage. It is important to remember that neurogenic fever is a diagnosis of exclusion.

Excellent biological arguments exist for a direct impact of fever specifically on neurological outcome. On a local level, fever produces increased levels of excitatory amino acids (e.g., glutamate and dopamine), free radicals, lactic acid, and pyruvate.22 There is an increase in cell depolarizations and BBB breakdown. Enzymatic function is impaired and cytoskeletal stability reduced. These events lead to increased cerebral edema, with a possible reduction in CPP as well as larger volumes of ischemic injury.23,24

A variety of brain injuries may be impacted by fever, including ischemic

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stroke, subarachnoid hemorrhage, , intracerebral hemorrhage, , traumatic brain injury,33 and global ischemic injury from cardiac arrest.34 Furthermore, the neuroprotective effects of hypothermia have been demonstrated for cardiac arrest patients35 and show promise in ischemic stroke patients as well.36

It appears that fever may worsen brain injury from any etiology, although it has yet to be shown that neurological outcome is directly influenced by hyperthermia. If such a link were established, it would further the case for aggressive fever control in neurologically injured patients. Although induced hypothermia has been shown to be effective in certain populations, it carries with it potential additional risks, including infection,37 coagulopathy, electrolyte imbalances,38 and cardiac dysrhythmias.39 Until hypothermia is proven to be effective, the goal of therapy should be maintenance of normothermia during the acute period of brain injury, thereby avoiding the potential harms of hyperthermia in this vulnerable time.

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