Neurologic clinics
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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.
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Cerebral dysfunction and injury in the ICU presents as focal neurologic deficits, seizures, coma, and delirium. These syndromes may result from a primary brain insult, such as stroke or trauma, but commonly are a complication of a systemic insult, such as cardiac arrest, hypoxemia, sepsis, metabolic derangements, and pharmacologic exposures. Many survivors of critical illness have cognitive impairment, which is believed to underlie the poor long-term functional status and quality of life observed in many critical illness survivors. Although progress has been made in characterizing the epidemiology of cerebral dysfunction in the ICU, more research is needed to elucidate underlying mechanisms that might represent targets for therapeutic intervention.
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Seizures and status epilepticus are common in critically ill patients. They can be difficult to recognize because most are nonconvulsive and require electroencephalogram monitoring to detect; hence, they are currently underdiagnosed. ⋯ Antiseizure medication should be combined with management of the underlying cause and reversal of factors that can lower the seizure threshold, including many medications, fever, hypoxia, and metabolic imbalances. This article discusses specific treatments and specific situations, such as hepatic and renal failure patients and organ transplant patients.
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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.