New horizons (Baltimore, Md.)
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Movement of water between the brain and the intravascular space is dependent on osmotic gradients, which may be established by the acute administration of either hyper- or hypo-osmolar solutions. Mannitol, a hypertonic crystalloid solution, is commonly used to decrease brain water content and reduce intracranial pressure (ICP). Hypertonic saline solutions also decrease brain water and ICP while temporarily increasing systolic blood pressure and cardiac output. ⋯ Colloid solutions exert little influence on either variable. Fluid restriction minimally affects cerebral edema and, if pursued to excess, may result in episodes of hypotension, which may increase ICP and are associated with worse neurologic outcome. Although there is no single best fluid for patients with traumatic brain injury, isotonic crystalloids are widely used and can be justified on a scientific basis.
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Knowledge of cerebral metabolic variables increases the information available for managing the head-injured patient. This article reviews normal cerebral metabolism and describes the derangement of metabolism observed in patients with head trauma. Cerebral metabolism is globally decreased by one third to one half in the severely head-injured patient, usually because of the lower metabolic expenditure associated with coma, but sometimes because of superimposed hypoxia/ischemia, primarily due to secondary insults. ⋯ Treatments can be directed at both increasing oxygen delivery and integrating hemodynamic handling, and at various pharmacologic or physical methods intended to reduce the cerebral metabolic demand. The latter strategy is designed to depress either the basal or activation components of cerebral metabolism. This strategy includes manipulations of brain temperature and the use of central nervous system-depressant, barbiturate, and similar drugs.
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In patients requiring ICP monitoring, a ventricular catheter connected to an external strain gauge transducer or catheter-tip pressure transducer device is the most accurate and reliable method of monitoring ICP, and enables therapeutic CSF drainage. Clinically significant infections or hemorrhage associated with ICP devices causing patient morbidity are rare and should not deter the decision to monitor ICP. ⋯ These devices are advantageous when ventricular ICP is not obtained or if there is obstruction in the fluid coupling. Subarachnoid or subdural fluid-coupled devices and epidural ICP devices are currently less accurate.
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Mannitol has replaced other diuretics as the agent of first choice for control of raised intracranial pressure (ICP) after brain injury. Mannitol should be given as a bolus intravenous infusion, over 10 to 30 mins, in doses ranging from 0.25 to 1.0 g/kg body weight. It may be given when high ICP is suspected, prior to computed tomography scanning, e.g., in patients who develop a fixed, dilated pupil or neurologic deterioration. ⋯ A Foley catheter should always be inserted when mannitol is used. Serum osmolality should be measured frequently after mannitol and maintained < 320 mOsm to avoid renal failure. Its beneficial effects and the rationale for its use are also reviewed.
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Head-injured patients require maintenance of systemic hemodynamics as well as attention to cerebral hemodynamics. Most head-injured patients have increased metabolic oxygen consumption, mild hypertension, and increased cardiac indices. Assessment of regional perfusion, difficult in many patients, includes monitoring of urinary output. In head-injured patients, especially those with multiple injuries, the two most important goals are preservation of cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) and maintenance of systemic oxygen availability (cardiac index times arterial oxygen content).