Neurocritical care
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In this article, we review technologies available for direct monitoring of cerebral oxygenation and metabolic status, including jugular venous oxygen saturation, brain tissue oxygen tension, transcranial cerebral oximetry with near-infrared spectroscopy, Positron emission tomography oxidative metabolism, single-photon emission computed tomography/computed tomography perfusion and functional imaging, and cerebral metabolite measurement using microdialysis. We also introduce a novel method of monitoring cerebral perfusion that may substitute for direct monitoring of oxygenation in the future.
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The development of animal models of acute stroke has allowed the evaluation of mild and moderate hypothermia as a therapeutic modality in this clinical setting. Studies have demonstrated that animals subjected to hypothermia up to 3 hours after the primary central nervous system insult have reduced mortality and neuronal injury, and improved neurological outcome. These results warranted the evaluation of hypothermia in clinical trials. ⋯ Thus, therapeutic hypothermia for ischemic stroke remains a promising but fiercely debated therapeutic modality. This review summarizes the animal model studies that have led to clinical trials in acute ischemic stroke. The existing techniques for inducing brain cooling, the mechanisms of neuroprotection, the complications of therapeutic hypothermia, and the future perspective of the field are also discussed.
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Severe intracranial hypertension (IH) in the setting of fulminant hepatic failure (FHF) carries a high mortality and is a challenging disease for the critical care provider. Despite considerable improvements in the understanding of the pathophysiology of cerebral edema during liver failure, therapeutic maneuvers that are currently available to treat this disease are limited. Orthotopic liver transplantation is currently the only definitive therapeutic strategy that improves outcomes in patients with FHF. ⋯ ICP monitoring, transcranial Doppler, and jugular venous oximetry offer valuable information regarding intracranial dynamics. Induced hypothermia, hypertonic saline, propofol sedation, and indomethacin are some of the newer therapies that have been shown to improve survival in patients with severe IH. In this article, we review the pathophysiology of IH in patients with FHF and outline various therapeutic strategies currently available in managing these patients in the critical care setting.
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Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH) is often referred to as "neurogenic stunned myocardium," which does not accurately reflect the suspected pathophysiology. We propose an alternative terminology, "neurogenic stress cardiomyopathy," as a more appropriate label based on our review of the current literature. ⋯ Recognition of the unique features associated with SAH-induced cardiac complications allows optimal management of patients with SAH. We will also discuss the clinical and theoretical overlap of SAH-induced cardiac dysfunction with a syndrome known as tako-tsubo cardiomyopathy and explore therapeutic opportunities.
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The combination of induced hypertension, hypervolemia, and hemodilution (triple-H therapy) is often utilized to prevent and treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Although this paradigm has gained widespread acceptance over the past 20 years, the efficacy of triple-H therapy and its precise role in the management of the acute phase of SAH remains uncertain. In addition, triple-H therapy may carry significant medical morbidity, including pulmonary edema, myocardial ischemia, hyponatremia, renal medullary washout, indwelling catheter-related complications, cerebral hemorrhage, and cerebral edema. This review examines the evidence underlying the implementation of triple-H therapy, and makes practical recommendations for the use of this therapy in patients with aneurysmal SAH.