Neurologic clinics
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Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. ⋯ For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.
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The devastating neurologic injury in survivors of cardiac arrest has been recognized since the development of modern resuscitation techniques. After numerous failed clinical trials, two trials showed that induced mild hypothermia can ameliorate brain injury and improve survival and functional neurologic outcome in comatose survivors of out-of-hospital cardiac arrest. This article provides a comprehensive review of the advances in the care of brain injury after cardiac arrest, with updates on the process of prognostication, the use of therapeutic hypothermia and adjunctive intensive care unit care for cardiac arrest survivors.
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Temperature management in acute neurologic disorders has received considerable attention in the last 2 decades. Numerous trials of hypothermia have been performed in patients with head injury, stroke, and cardiac arrest. ⋯ Detrimental effects of fever and benefits of normalizing elevated temperature in experimental models are discussed. This article presents a detailed analysis of trials of induced hypothermia in patients with acute neurologic insults and describes methods of fever control.
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Mechanical ventilation (MV) is fundamental to the resuscitation of brain injured patients, facilitating tissue oxygen delivery, helping to modulate cerebral vascular reactivity, and ensuring protection of the airway. These benefits come at a cost, which includes a significantly increased risk of pneumonia, delirium, and the complications of sedation and of endotracheal intubation. ⋯ MV can also induce alveolar damage in susceptible individuals, yet changes in ventilation designed to limit this damage may not be tolerated in the setting of brain injury. Recent research has begun to clarify key questions regarding the pathophysiology and management of MV in critically ill neurological patients.
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Critical illness neuromyopathy (CINM) is suggested by bilateral diffuse weakness predominant in the proximal part of the limbs after improvement of the acute phase of critical illness. Although muscle and peripheral nerve are often involved in combination, muscle involvement alone is increasingly identified on electrophysiologic investigation, including direct muscle stimulation. CINM frequently involves the respiratory muscles and may result in delayed weaning and prolonged mechanical ventilation. Besides muscle immobilization and prolonged sepsis-induced multiorgan failure, which are risk factors for CINM, hyperglycemia and use of corticosteroids might have a deleterious effect on the neuromuscular system in critically ill patients, suggesting opportunities for preventive interventions.