Neurologic clinics
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Considerable progress has been made in providing high-quality prehospital and emergency cardiac care for OHCA victims. The use of early CPR, early defibrillation, early ACLS, and state-of-the-art postresuscitation care offers the best promise for improved community survival and neurologic outcome statistics in the future. The NIH-sponsored Resuscitation Outcomes Consortium represents the largest governmentally sponsored effort of its kind that that will test the value of promising pharmacologic and device interventions on improving survival and neurologic outcome in OHCA patients.
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The use of IH for 24 hours in patients who remain comatose following resuscitation from out-of-hospital cardiac arrest improves outcomes. How-ever, the induction of hypothermia has several physiologic effects that need to be considered. ⋯ Hypothermia (33 degrees C) should be maintained for 24 hours, followed by rewarming over 12 hours. Particular attention must be paid to potassium and glucose levels during hypothermia.
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Intensive care technologies have led to an increase in patients who are neurologically devastated and deceased. The practical, moral, and ethical situations encountered can be varied and challenging to manage. Decisions and discussions surrounding withdrawal of care, death by neurologic criteria, and organ donation require significant knowledge of the prognosis, ancillary testing, and definitions of these processes. Experience and skill are often required on the part of physicians and staff to guide families through these most difficult of circumstances.
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It is difficult to predict precisely the final neurologic outcome from cardiac arrest and accompanying cerebral hypoxia. Although rare, several movement disorders may arise as a consequence of hypoxic injury, including myoclonus, dystonia, akinetic-rigid syndromes, tremor, and chorea. ⋯ Many outstanding questions remain, however. What factors promote susceptibility to the development of posthypoxic movement disorders? Why do patients who have similar clinical hypoxic insults develop markedly dis-similar movement disorders? Why are the basal ganglia especially vulnerable to cerebral hypoxia? Why do some movement disorders occur in delayed fashion and progress for years after the hypoxic insult? Is the pathogenesis of progressive posthypoxic movement disorders related to that of neurodegenerative diseases? What are the most effective medications for the various posthypoxic movement disorders? Is there a role for deep brain stimulation in the treatment of posthypoxic movement disorders? We anticipate that current and future research in the area of posthypoxic movement disorders will reveal answers to some of these important questions.
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Nocturnal sleep-related ventilatory alterations may occur in dis-proportion to the severity of the neuromuscular disorder. Diaphragm paralysis occurring with a neuromuscular disorder is an overlooked complication. ⋯ Polysomnographic evaluation is recommended for patients who have neuromuscular disorder who develop symptoms and signs of sleep-wake abnormality or nocturnal respiratory failure. Application of noninvasive positive airway ventilation and, in some cases, administration of supple-mental oxygen may improve quality of life and prolong survival of patients who have neuromuscular disorder.