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Disorders of Consciousness
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Targeted temperature management (TTM) to 32–36°C for at least 24 hours in comatose survivors of cardiac arrest may improve neurologic outcome. The benefit was first demonstrated in patients with out-of-hospital cardiac arrest (OHCA) with a shockable cardiac rhythm, and TTM to 36°C was ultimately shown to be as effective as 33°C in this population.17–19 The evidence supporting TTM after in-hospital cardiac arrest and in patients with nonshockable rhythm is growing and supported by several societal guidelines.20,21 Induction of hypothermia can be instituted with IV ice-cold fluids or ice packs on the groin, armpits, neck, and head. Surface or IV cooling devices can also be used. Maintenance of hypothermia is best achieved with external or internal cooling devices with continuous temperature feedback to achieve the desired target temperature. Slow rewarming at 0.25–0.5°C per hour is recommended. Shivering can be treated with sedation and neuromuscular blockade.
Cardiopulmonary Resuscitation in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, Cardio-Obstetrics, 2020
The AHA 2015 guidelines explicitly state, “There are essentially no patients for whom temperature control somewhere in the range between 32°C and 36°C is contraindicated,” and recommends targeted temperature management (TTM) for at least 24 hours following return of spontaneous circulation after cardiac arrest [85]. Data specific to TTM in pregnancy remain limited to case reports [87–92], but there have been some successful maternal outcomes. Information on the perinatal outcome with post-arrest TTM use in an ongoing pregnancy is more limited. Fetal heart rate monitoring may show fetal bradycardia in response to maternal hypothermia [91], but this is likely to resolve as rewarming occurs.
Basic Thermal Physiology: What Processes Lead to the Temperature Distribution on the Skin Surface
Published in Kurt Ammer, Francis Ring, The Thermal Human Body, 2019
Since a variety of temperature targets are now used, the 2015 updated American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care adopted the term targeted temperature management to refer to induced hypothermia as well as to active control of temperature at any target [137]. The following three recommendations are made: It is recommended that comatose (i.e. lack of meaningful response to verbal commands) adult patients with return of spontaneous circulation after cardiac arrest have targeted temperature management. This applies to the subgroup of patients with out-of-hospital cardiac arrest due to ventricular fibrillation/pulse less ventricular tachycardia and to patients within-hospital cardiac arrest caused non-ventricular fibrillation/ pulse less ventricular tachycardia.The guideline recommends selecting and maintaining a constant temperature between 32°C and 36°C during targeted temperature management.The third recommendation is against the routine pre-hospital cooling of patients after return of spontaneous circulation with rapid infusion of cold intravenous fluids.
Mild Hypothermia via External Cooling Improves Lung Function and Alleviates Pulmonary Inflammatory Response and Damage in Two-Hit Rabbit Model of Acute Lung Injury
Published in Journal of Investigative Surgery, 2022
Onat Akyol, Serdar Demirgan, Aslıhan Şengelen, Hasan Cem Güneyli, Duygu Sultan Oran, Funda Yıldırım, Damla Haktanır, Mehmet Salih Sevdi, Kerem Erkalp, Ayşin Selcan
Hypothermic targeted temperature management (TTM) is an area of ongoing investigation for several different medical conditions (27, 28). It is the most established clinical application in patients after cardiac arrest. In critical care medicine, it is recommended to maintain the core body temperature of 32–34 °C for comatose patients after cardiac arrest (11). Besides the post-cardiac arrest situation, several experimental studies documented beneficial outcomes by therapeutic hypothermia, especially in different brain injury animal models (9). Apart from these, various experimental and clinical studies reported the protective effects of hypothermia in lung injury, pneumonia, and COVID-19 (12–15). Significant molecular mechanisms of controlled therapeutic hypothermia (TH) include the modulating and suppressing the mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), and tumor necrosis factor-alpha (TNF-α) pathways, ameliorating inflammation, decreasing free radical generation, inhibiting excitotoxicity and apoptosis, and slowing down of metabolism. Importantly, hypothermia plays a protective role during the inflammatory response by suppressing the inflammatory cascade and decreasing nitric oxide, cytokine, and leukotriene production (8, 29–31). In addition, some studies have revealed that action mechanism of TH include the improvement of gas exchange and lung mechanics in patients (15, 32, 33).
Acute kidney injury and cardiac arrest in the modern era: an updated systematic review and meta-analysis
Published in Hospital Practice, 2021
Narut Prasitlumkum, Wisit Cheungpasitporn, Ryota Sato, Ronpichai Chokesuwattanaskul, Charat Thongprayoon, Sri Harsha Patlolla, Tarun Bathini, Michael A Mao, S Tanveer Rab, Kianoush Kashani, Saraschandra Vallabhajosyula
A total of 1,428 potentially eligible articles were identified using our search strategy, of which 25 studies encompassing 8,165 patients met the inclusion criteria (Figure 1). Of these, 18 were retrospective cohort studies, five prospective cohort studies, one randomized control trial, and one cross-sectional study. The characteristics and quality assessment of the included studies are presented in Table 1. The AKI incidence ranged from 10%-60%. In the included studies, the populations were mainly male (62.8%), with an average age of 61.7 ± 13.3 years. The setting for the majority of CAs was out-of-hospital CA, which was often used as part of the inclusion criteria. Acute kidney injury network (AKIN), Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease (RIFLE), and Kidney Disease Improving Global Outcomes (KDIGO) were all employed as an AKI definition [18–20]. Targeted temperature management (TTM) protocols were inconsistently used in the studies with a varying incidence of 38.6–100%. Rhythm status and cardiogenic causes of CA are described in Table 1. The Newcastle–Ottawa Scale ranged from 5 to 8, indicating moderate to high quality of included studies (Online supplementary file).
Thermoregulation: From basic neuroscience to clinical neurology, part 2
Published in Temperature, 2019
Zoltán Szelényi, Sámuel Komoly
Chapter 48, authored by Robert D. Fealey, deals with thermoregulation in neuropathies. It is a useful, comprehensive source of new data related to thermoregulatory sweating impairment in neuropathy. Chapter 49, by Ram Gowda, Matthew Jaffa and Neeraj Badjatia, deals with thermoregulation in brain injury. The major message of the chapter is that targeted temperature management trials, unfortunately, were not effective in decreasing brain damage in traumatic brain injury or stroke, whether ischemic or hemorrhagic. Despite the negative results of these trials, the targeted temperature management approach continues to be investigated in clinical trials (see also chapter 51). Chapter 50, authored by Mike J. Price1 and Michelle Trbovich, deals with thermoregulation following spinal cord injury. It is evident that there is a reduced afferent input to the brain and a decrease in the efferent output to thermoeffectors (cutaneous vasomotor and sweating) below the level of spinal cord lesion. The chapter ends with a message that physical fitness is an important component in decreasing dysfunctions of thermoregulation in patients with spinal cord injury.