Decompressive craniotomy can increase the size of the cranium, although this surgical intervention is controversial. Anecdotal evidence suggests that it may be useful in young patients with initially high GCS who deteriorate due to severe brain edema. Decompressive procedures generally include wide frontal, temporal and parietal craniotomies with augmentation duraplasty to allow for the temporary expansion of edematous brain without secondary increases in ICP.
Although most therapeutic interventions for intracranial hypertension focus on maintaining adequate supply (i.e., cerebral blood flow), a few are directed towards reducing demand (i.e., brain metabolic rate). Hypothermia reduces the cerebral metabolic rate and cerebral blood flow and also lowers ICP. Deep hypothermia (30 degrees C) also increases the incidence of cardiac arrhythmia and other complications. Although controversial, moderate hypothermia (32 to 34 deg. C) has shown beneficial effects in some clinical trials. Hyperthermia, conversely, increases brain metabolism and ICP and is deleterious to brain injured patients. Antipyretics and active cooling may be used to maintain normothermia to mild hypothermia.
Continuous infusion of barbiturate drugs (often pentobarbital) results in decreased cerebral blood volume, cerebral metabolic rate and ICP. Barbiturates also depress the peripheral circulatory system and systemic blood pressure, potentially decreasing cerebral blood flow. Therefore, barbiturate therapy is reserved for refractory intracranial hypertension and requires close monitoring by the critical-care team. EEG monitoring is required to monitor burst suppression, and invasive hemody-namic monitoring is required to avoid hypotension. The duration of therapy is generally several days to over a week.
Finally, a number of drugs have been developed to reduce the metabolic cascade of secondary tissue injury after brain trauma. Calcium-channel blockers, such as nimodepine, may prevent calcium-mediated neuronal damage or prevent ischemic vasospasm due to traumatic subarachnoid hemorrhage. Glutamate antagonists and antioxidative agents may protect neurons from transmitter-induced and hypoxic membrane damage. However, most clinical trials of these agents have been performed in adults, and few have shown promise even in that setting. The use of nimodepine for head injury in children is controversial.
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