New horizons (Baltimore, Md.)
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Moderate systemic hypothermia has been shown to improve neurologic outcomes in both fluid-percussion and cortical contusion models of experimental brain injury. Based upon initial clinical work, it was concluded that at temperatures < 32 degrees C, patients with severe brain injury were at increased risk of ventricular arrhythmias, and that rapid rewarming immediately postinjury predisposed to intracranial pressure increases. Subsequent clinical studies of moderate hypothermia (32 degrees C) for 24- to 48-hr duration with slow rewarming in human brain injury showed indications of neurologic improvement and a low incidence of hypothermia-related complications. ⋯ The efficacy of hyperbaric oxygen administered every 8 hrs for 1-hr duration for a 2-wk period has also been tested in patients after severe brain injury. While the mortality rate was reduced in the treated group, the percentage of favorable outcomes was unchanged. Further studies are in progress.
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Sedative and neuromuscular blocking (NMB) drugs are used to facilitate care of head trauma patients requiring mechanical ventilation or therapy of intracranial hypertension. Because no specific regimen is appropriate in all patients, drug selection and utilization exhibit significant regional variation. Sedatives are used to decrease anxiety and diminish awareness of noxious stimuli. ⋯ Increasingly more information is available to guide the use of NMB drugs for patients suffering head trauma. Broad concerns about these drugs include their use as adjunctive therapy to control intracranial hypertension, the incidence of prolonged weakness or myopathy, the potential for direct neurologic toxicity, and their effect on outcome. Resolution of these issues will improve the use of sedative and NMB drugs in intensive care.
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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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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).