Neurocritical care
-
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.
-
The acceptance of brain death by society has allowed for the discontinuation of "life support" and the transplantation of organs. The standard clinical criteria for brain death, when rigorously applied, ensure that the brainstem is destroyed. Because more rostral structures are more vulnerable than the brainstem, these are almost invariably devastated when brainstem function is irreversibly lost as a result of whole brain insults. ⋯ Ancillary tests are also required in very young children. In addition, some societies require their use as a matter of principle. Only tests of whole-brain perfusion adequately serve these purposes.
-
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.
-
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.
-
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.