Neurocritical care
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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.
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Guillain-Barré Syndrome is the leading cause of nontraumatic acute paralysis in industrialized countries. About 30% of patients have respiratory failure requiring intensive care unit (ICU) admission and invasive mechanical ventilation. Progressive weakness of both the inspiratory and the expiratory muscles is the mechanism leading to respiratory failure. ⋯ They include rapidly progressive motor weakness, involvement of both the peripheral limb and the axial muscles, ineffective cough, bulbar muscle weakness, and a rapid decrease in vital capacity. Specific treatments (plasma exchange and intravenous immunoglobulins) have decreased both the number of patients requiring ventilation and the duration of ventilation. The need for mechanical ventilation is associated with residual functional impairments, although all patients eventually recover normal respiratory muscle function.
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Excessive hypertension can challenge the brain's capacity to autoregulate cerebral blood flow, and can aggravate increased intracranial pressure (ICP) and cerebral edema. Hypotension may worsen ischemic damage in marginally perfused tissue, and in some cases can trigger cerebral vasodilation and ICP plateau waves. There is a lack of high-quality data regarding optimal BP management in these conditions. ⋯ To reduce BP, labetalol, esmolol, and nicardipine best meet these criteria. Sodium nitroprusside should be avoided in most neurological emergencies because of its tendency to raise ICP and cause toxicity with prolonged infusion. To elevate BP, the preferred agents are phenylephrine, dopamine, and norepinephrine.
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Experimental evidence and clinical experience suggest that mild hypothermia protects numerous tissues from damage during ischemic insult. However, the extent to which hypothermia becomes a valued therapeutic option will depend on the clinician's ability to rapidly reduce core body temperature and safely maintain hypothermia. To date, general anesthesia is the best way to block autonomic defenses during induction of mild-to-moderate hypothermia; unfortunately, general anesthesia is not an option in most patients likely to benefit from therapeutic hypothermia. ⋯ In an effort to inhibit thermoregulation in awake humans, several agents have been tested either alone or in combination with each other. For example, the combination of meperidine and buspirone has already been applied to facilitate induction of hypothermia in human trials. However, pharmacological induction of thermoregulatory tolerance to cold without excessive sedation, respiratory depression, or other serious toxicity remains a major focus of current therapeutic hypothermia research.
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This review examines the available data on the use of osmotic agents in patients with head injury and ischemic stroke, summarizes the physiological effects of osmotic agents, and presents the leading hypotheses regarding the mechanism by which they reduce ICP. Finally, it addresses the validity of the following commonly held beliefs: mannitol accumulates in injured brain; mannitol shrinks only normal brain and can increase midline shift; osmolality can be used to monitor mannitol administration; mannitol should be not be administered if osmolality is >320 mOsm; and hypertonic saline is equally effective as mannitol.