The Experts below are selected from a list of 258 Experts worldwide ranked by ideXlab platform

Christopher Zacko - One of the best experts on this subject based on the ideXlab platform.

  • guidelines for the acute treatment of Cerebral Edema in neurocritical care patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Morgan G Jones, Christopher Zacko
    Abstract:

    Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.

  • Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, G. Morgan Jones, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Christopher Zacko
    Abstract:

    Background Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. Methods The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. Results The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. Conclusion The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.

Marc J Simard - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Edema after cardiopulmonary resuscitation a therapeutic target following cardiac arrest
    Neurocritical Care, 2018
    Co-Authors: Erik G Hayman, Kevin N Sheth, Akil P Patel, Taylor W Kimberly, Marc J Simard
    Abstract:

    We sought to review the role that Cerebral Edema plays in neurologic outcome following cardiac arrest, to understand whether Cerebral Edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, Cerebral Edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. Like other conditions characterized by Cerebral ischemia/reperfusion, neuroprotection after cardiac arrest has proven to be difficult to achieve. Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood–brain barrier. Limited preclinical data suggest that strategies to reduce Cerebral Edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting Cerebral Edema will improve patient outcomes after cardiac arrest.

  • mechanisms of global Cerebral Edema formation in aneurysmal subarachnoid hemorrhage
    Neurocritical Care, 2017
    Co-Authors: Erik G Hayman, Volodymyr Gerzanich, Aaron Wessell, Kevin N Sheth, Marc J Simard
    Abstract:

    A growing body of clinical literature emphasizes the impact of Cerebral Edema in early brain injury following aneurysmal subarachnoid hemorrhage (aSAH). Aneurysm rupture itself initiates global Cerebral Edema in up to two thirds of cases. Although Cerebral Edema is not a universal feature of aSAH, it portends a poor clinical course, with quantitative analysis revealing a direct correlation between Cerebral Edema and poor outcome, including mortality and cognitive deficits. Mechanistically, global Cerebral Edema has been linked to global ischemia at the time of aneurysm rupture, dysfunction of autoregulation, blood breakdown products, neuroinflammation, and hyponatremia/endocrine abnormalities. At a molecular level, several culprits have been identified, including aquaporin-4, matrix metalloproteinase-9, SUR1-TRPM4 cation channels, vascular endothelial growth factor, bradykinin, and others. Here, we review these cellular and molecular mechanisms of global Cerebral Edema formation in aSAH. Given the importance of Edema to the outcome of patients with aSAH and its status as a highly modifiable pathological process, a better understanding of Cerebral Edema in aSAH promises to hasten the development of medical therapies to improve outcomes in this frequently devastating disease.

  • molecular pathophysiology of Cerebral Edema
    Journal of Cerebral Blood Flow and Metabolism, 2016
    Co-Authors: Jesse A Stokum, Volodymyr Gerzanich, Marc J Simard
    Abstract:

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating Cerebral Edema. In large part, the study of Cerebral Edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as Cerebral Edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of Cerebral Edema.

Aaron M. Cook - One of the best experts on this subject based on the ideXlab platform.

  • guidelines for the acute treatment of Cerebral Edema in neurocritical care patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Morgan G Jones, Christopher Zacko
    Abstract:

    Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.

  • Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, G. Morgan Jones, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Christopher Zacko
    Abstract:

    Background Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. Methods The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. Results The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. Conclusion The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.

Geoffrey T Manley - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Edema in traumatic brain injury pathophysiology and prospective therapeutic targets
    Neurosurgery Clinics of North America, 2016
    Co-Authors: Geoffrey T Manley, Ethan A Winkler, Daniel J Minter
    Abstract:

    : Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of Cerebral Edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of Cerebral Edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying Cerebral Edema and highlight the molecular pathways that may be therapeutically targeted to mitigate Cerebral Edema and associated sequelae following traumatic brain injury.

  • role of aquaporin 4 in Cerebral Edema and stroke
    Handbook of experimental pharmacology, 2009
    Co-Authors: Zsolt Zador, Shirley I Stiver, Vincent Y Wang, Geoffrey T Manley
    Abstract:

    Cerebral Edema plays a central role in the pathophysiology of many diseases of the central nervous system (CNS) including ischemia, trauma, tumors, inflammation, and metabolic disturbances. The formation of Cerebral Edema results in an increase in tissue water content and brain swelling which, if unchecked, can lead to elevated intracranial pressure (ICP), reduced Cerebral blood flow, and ultimately Cerebral herniation and death. Despite the clinical significance of Cerebral Edema, the mechanism of brain water transport and Edema formation remain poorly understood. As a result, current therapeutic tools for managing Cerebral Edema have changed little in the past 90 years. “Malignant ischemic stroke” is characterized by high mortality (~80%) and represents a major clinical problem in cerebrovascular disease. Widespread ischemic injury in these patients causes progressive Cerebral Edema, increased ICP, and rapid clinical decline. In response to these observations, a series of recent studies have begun to target Cerebral Edema in the management of large ischemic strokes. During Cerebral Edema formation, the glial water channel aquaporin-4 (AQP4) has been show to facilitate astrocyte swelling (“cytotoxic swelling”). AQP4 has also been seen to be responsible for the reabsorption of extracellular Edema fluid (“vasogenic Edema”). In the present review, the role of AQP4 in the development of Cerebral Edema is discussed with emphasis on its contribution to ischemic Edema. We also examine the potential of AQP4 as a therapeutic target in Edema associated with stroke.

Chitra Venkatasubramanian - One of the best experts on this subject based on the ideXlab platform.

  • guidelines for the acute treatment of Cerebral Edema in neurocritical care patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Morgan G Jones, Christopher Zacko
    Abstract:

    Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.

  • Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients
    Neurocritical Care, 2020
    Co-Authors: Aaron M. Cook, G. Morgan Jones, Gregory W. J. Hawryluk, Patrick Mailloux, Diane Mclaughlin, Alexander Papangelou, Sophie Samuel, Sheri Tokumaru, Chitra Venkatasubramanian, Christopher Zacko
    Abstract:

    Background Acute treatment of Cerebral Edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of Cerebral Edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of Cerebral Edema. Clinicians must be able to select appropriate therapies for initial Cerebral Edema management based on available evidence while balancing efficacy and safety. Methods The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of Cerebral Edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. Results The panel generated recommendations regarding initial management of Cerebral Edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intraCerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. Conclusion The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or Cerebral Edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing Cerebral Edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with Cerebral Edema.