Neurocritical care
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Aneurysmal subarachnoid hemorrhage (SAH) affects 30,000 patients per year, causing neurologic morbidity and mortality. The etiology of hypoxemia and its role in comorbidity are controversial and unknown. ⋯ Oxygenation abnormalities after SAH occur more frequently than previously suspected. They are frequently the result of noncardiogenic and hydrostatic causes and contribute to an increased length of hospital stay.
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Recent evidence suggests that magnesium may be neuroprotective in the setting of cerebral ischemia, and therapeutic magnesium infusion has been proposed for prophylaxis and treatment of delayed ischemic neurological deficit (DIND) resulting from vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). We studied the association between serum magnesium levels, the development of DIND, and the outcomes of patients with SAH. ⋯ We identified no relationship between serum magnesium levels and the development of DIND or outcome following aneurysmal SAH. Based on these data, magnesium supplementation to normal or high-normal physiological ranges seems unlikely to be beneficial for DIND resulting from vasospasm. However, no inference can be made regarding the value of therapeutic infusion of magnesium to supraphysiological levels.
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Use of hypertonic saline (HTS) is gaining acceptance in the neurosciences critical care unit (NCCU) based on its efficacy in reducing cerebral edema and its favorable hemodynamic profile. In the NCCU, unfamiliarity with the use of HTS may result in implementation difficulties. We report our initial experience using HTS, its ability to achieve a hypernatremic state, and adverse effects. ⋯ The use of HTS for cerebral edema requires intensive efforts by the medical team to rapidly achieve and maintain a hypernatremic state. The continuous infusion of HTS was used safely.
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It is controversial whether a low cerebral blood flow (CBF) simply reflects the severity of injury or whether ischemia contributes to the brain's injury. It is also not clear whether posttraumatic cerebral hypoperfusion results from intracranial hypertension or from pathologic changes of the cerebral vasculature. The answers to these questions have important implications for whether and how to treat a low CBF. ⋯ In patients with CBF<18 mL/100 g/minutes, intracranial hypertension plays a major causative role in the reduction in CBF. Treatment would most likely be directed at controlling intracranial pressure, but the early, severe intracranial hypertension also probably indicates a severe brain injury. For levels of CBF between 18 and 40 mL/100 g/minutes, the presence of regional hypoperfusion was a more important factor in reducing the average CBF.
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A common observation in closed head injuries is the contrecoup brain injury. As the in vivo brain is less dense than the cerebrospinal fluid (CSF), one hypothesis explaining this observation is that upon skull impact, the denser CSF moves toward the site of skull impact displacing the brain in the opposite direction, such that the initial impact of the brain parenchyma is at the contrecoup location. ⋯ The pattern of brain injury in which the contrecoup injury is greater than the coup injury is a result of initial movement of the brain in the contrecoup location. During the process of closed head injury, the brain parenchyma is initially displaced away from the site of skull impact and toward the contrecoup site resulting in the more severe brain contusion.