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A second panel discussion covers managing hypothermia in cardiac arrest patients, especially during the rewarming phase. The development of a highly successful hypothermia program in a community hospital is described as well as the use of hypothermia in complex multicenter trials involving cardiac arrest and in patients undergoing aneurysm surgery. The use of surrogate markers that could aid in the assessment of the status of the brain during the cooling and rewarming phases is also emphasized. Interest in using therapeutic hypothermia and temperature management strategies during various emergency sessions continues to grow.
An editorial commentary on an article by Tang and colleagues, previously published in Volume 3, Number 2 (2013), is also included in this issue. The original article, “Mild Hypothermia Reduces Tissue Plasminogen Activator-Related Hemorrhage and Blood Brain Barrier Disruption after Experimental Stroke” is of interest in the field of stroke treatments. In this informative editorial commentary, Patrick Lyden, MD, provides a perspective on thrombolysis with stroke and emphasizes the useful information that can be gained from preclinical studies testing thrombolytic or hypothermia treatments. The observation that hypothermia may reduce hemorrhagic risk during thrombolysis is important to the field and provides a solid basis for clinical studies in which temperature management and thrombolytic treatments are being evaluated.
In an original article by Raper and Wang, changes in urine output during post–cardiac arrest therapeutic hypothermia are emphasized. Mean urine output rates during induction, maintenance, rewarming, and post-rewarming phases were compared. The authors observed a modest increase in urine output in patients during therapeutic hypothermia treatment.
In another original article, Gregerson and colleagues describe the limitations of mild, moderate, and profound hypothermia in protecting and developing hippocampal neurons following a simulated ischemic insult. The authors emphasize that ischemic severity and when hypothermia is initiated are important variables in determining whether hypothermia is protective in saving neurons from a hypoxic/ischemic insult. These preclinical data emphasize the potential limitations of therapeutic hypothermia in models of severe injury as well as when early treatments cannot be initiated. In a third original article, Kawabori and colleagues report the interesting effect of hypothermia on triggering receptors expressed on myelloid cells-2 (TRIM 2), a newly identified surface receptor shown to be involved in phagocytosis. Previous studies have reported that temperature has significant effects on inflammatory cascades as well as phagocytosis. This study reports that the proportion of TRIM-2 positive microglia/macrophages was increased during early hypothermia in a model of middle cerebral artery occlusion in mice. These observations emphasize that TRIM-2 and other mechanisms involved in phagocytosis may have a beneficial role in brain ischemia.
One case report is also included in this issue that describes Beau's lines after cardiac arrest in a 34-year-old male with uncontrolled hypertension who underwent therapeutic hypothermia treatment. The case report describes a lengthy post-arrest clinical course complicated by a variety of clinical problems. Physical examination identified Beau's lines on the individual's fingernails that may emphasize a component of his clinical history.
Our special Arctic Challenge section of the Journal addresses questions currently being asked regarding strategies and risk factors associated with cooling in various patient populations. In this issue, some questions include how to start and stop cooling once a patient reaches goal temperature. Another question addresses hemodilution methods for cardiac arrest evaluation and how these are modified during a therapeutic hypothermia protocol. Whether there is any evidence showing beneficial effects of therapeutic hypothermia for in-hospital cardiac arrest is discussed. Future studies focusing on in-hospital cardiac arrest and the benefits of therapeutic hypothermia need to be conducted. An important clinical question remains regarding the use of therapeutic hypothermia in patients that demonstrate no brain stem reflexes after they are rewarmed. This is a complicated patient group in which therapeutic hypothermia can be a confounder in the determination of brain death using standard protocols. Handling cooling-related bradycardia and determining how low is too low is another common question that is brought up during cooling strategies. The authors emphasize that each patient should be individually assessed to determine the effects of cooling on the impact of hemodynamics and cardiac function.
An important function of our Journal is to provide up-to-date information on the latest topics discussed by the scientific community at national and international meetings in the field of temperature management. An important series of abstracts presented at this year's 3rd Annual Innsbruck Temperature Management Meeting are provided in this issue. These abstracts provide the reader with a summary of timely communications by authorities on hypothermia research.
We thank the authors for their high-quality submissions and for considering our Journal as a prime venue to present their new work. As editor-in-chief, I hope you are enjoying the Journal and that you continue to support the continued growth of this publication. If you have any questions or would like to submit a letter to the editor or any other type of communication addressing our articles, please contact me.