Relevant bibliographies by topics / Hypothermia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Hypothermia'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Hypothermia"

1

Tomcsányi, János, Péter Arányi, and Hrisula Arabadzisz. "Terápiás hypothermia okozta QT-megnyúlás és „torsade de pointes” kamrai tachycardia." Orvosi Hetilap 163, no. 13 (March 27, 2022): 523–26. http://dx.doi.org/10.1556/650.2022.32367.

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Összefoglaló. A szerzők egy 44 éves, autoimmun betegségben szenvedő nőbeteg kórlefolyását ismertetik. A váratlan kórházi kamrafibrillációt követő sikeres resuscitatio után a beteg comatosus állapotban maradt, ezért terápiás hypothermiában részesült. A hypothermiás kezelés hatására jelentős QT-megnyúlás és „torsade de pointes” kamrai tachycardia lépett fel. A hypothermia okozta szívritmuszavar oka a hőmérséklet-csökkenés kiváltotta QT-megnyúlás és korai utódepolarizációs mechanizmusú triggerelt aktivitás. A szerzők felhívják a figyelmet arra, hogy jelen tudásunk szerint enyhe hypothermiát javasolt alkalmazni az ajánlásban szereplő hypothermiás tartományon belül. Orv Hetil. 2022; 163(13): 523–526. Summary. The authors describe the course of disease in a 44-year-old female patient with autoimmune disease. After successful resuscitation following unexpected hospital ventricular fibrillation, the patient remained in a comatose state and therefore received therapeutic hypothermia. Hypothermic treatment resulted in significant QT prolongation and „torsade de pointes” ventricular tachycardia. The probable cause of arrhythmia is the QT prolongation caused by the hypothermia and the consequential early afterdepolarization and triggered activity. The authors draw attention to the fact that – to the best of our knowledge – milder hypothermia is recommended within the preset hypothermic range. Orv Hetil. 2022; 163(13): 523–526.
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Gao, Guoyi, Yasutaka Oda, Enoch P. Wei, and John T. Povlishock. "The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat." Journal of Cerebral Blood Flow & Metabolism 30, no. 3 (November 11, 2009): 628–37. http://dx.doi.org/10.1038/jcbfm.2009.235.

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This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.
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McHugh, Michael, Brian Conway, Marcos Nores, and Sotiris Stamou. "Role of Moderate Hypothermia and Antegrade Cerebral Perfusion during Repair of Type A Aortic Dissection." International Journal of Angiology 27, no. 04 (October 29, 2018): 190–95. http://dx.doi.org/10.1055/s-0038-1675204.

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The goal of this study was to compare early postoperative outcomes and actuarial survival between patients who underwent repair of acute type A aortic dissection with deep or moderate hypothermia.A total of 132 consecutive patients from a single academic medical center underwent repair of acute type A aortic dissection between January 2000 and June 2014. Of those, 105 patients were repaired under deep hypothermia (< 24 C°), while 27 patients were repaired under moderate hypothermia (≥24 C°). Median ages were 62 years (range: 27–86) and 59 years (range: 35–83) for patients repaired under deep hypothermia compared with patients repaired under moderate hypothermia, respectively (p = 0.451). Major morbidity, operative mortality, and 10-year actuarial survival were compared between groups.Operative mortality was 17.1 and 7.4% in the deep and moderate hypothermia groups, respectively (p = 0.208). Incidence of permanent stroke was 12.4% in the deep hypothermic circulatory arrest group and 0% in the moderate hypothermia group (p = 0.054). Actuarial 5- and 10-year survival demonstrated a trend for lower long-term mortality with moderate hypothermia compared with deep hypothermia (69% 5-year and 54% 10-year for deep hypothermia vs. 79% 5-year and 10-year for moderate hypothermia, log-rank p = 0.161).Moderate hypothermia is a safe and efficient alternative to deep hypothermia and may have protective benefits. Stroke rate was lower with moderate hypothermia.
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Arif, Khamid, and Etlidawati Etlidawati. "Jenis Anastesi Dengan Kejadian Hipotermi Di Ruang Pemulihan RSUD Banyumas." Adi Husada Nursing Journal 7, no. 1 (August 26, 2021): 41. http://dx.doi.org/10.37036/ahnj.v7i1.189.

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Cases that often occur after the distinction in the recovery room one of them is hypothermy. One of the causes of postoperative hypothermy is the type of anaesthetic used. The purpose of the study was to find out the relationship of anaesthetic type to the incidence of hypothermic. Research design uses correlational with cross sectional approaches. The population of all postoperative patients in the Recovery Room of Banyumas Hospital over the past 3 months as many as 500 patients. A large sample of 83 patients using consecutive sampling techniques. The research instrument used is an observation sheet to record the type of anaesthetic and body temperature. Data analysis using the chi square test. Patients mostly respondents aged 36-46 years as many as 51 respondents (61.4%), men as many as 52 respondents (62.7%) and high school / vocational education as many as 39 respondents (47.0%). Respondents received general anaesthetics of 58 respondents (69.9%) and hypothermi as many as 60 respondents (72.3%). Statustic test results obtained a value of p = 0.000 which showed there was a relationship of anaesthetic type with the incidence of hypothermi in the Recovery Room of Banyumas Hospital. The type of anaesthetic used can determine the occurrence of changes in body temperature, namely hypothermy. Keywords: anesthesia, hypothermia, recovery room
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Oh, Joo Suk, Jungtaek Park, Kiwook Kim, Hyun Ho Jeong, Young Min Oh, Semin Choi, and Kyoung Ho Choi. "HSP70-mediated neuroprotection by combined treatment of valproic acid with hypothermia in a rat asphyxial cardiac arrest model." PLOS ONE 16, no. 6 (June 17, 2021): e0253328. http://dx.doi.org/10.1371/journal.pone.0253328.

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It has been reported that valproic acid (VPA) combined with therapeutic hypothermia can improve survival and neurologic outcomes in a rat asphyxial cardiac arrest model. However, neuroprotective mechanisms of such combined treatment of valproic acid with hypothermia remains unclear. We hypothesized that epigenetic regulation of HSP70 by histone acetylation could increase HSP70-mediated neuroprotection suppressed under hypothermia. Male Sprague-Dawley rats that achieved return of spontaneous circulation (ROSC) from asphyxial cardiac arrest were randomized to four groups: normothermia (37°C ± 1°C), hypothermia (33°C ± 1°C), normothermia + VPA (300 mg/kg IV initiated 5 minutes post-ROSC and infused over 20 min), and hypothermia + VPA. Three hours after ROSC, acetyl-histone H3 was highly expressed in VPA-administered groups (normothermia + VPA, hypothermia + VPA). Four hours after ROSC, HSP70 mRNA expression levels were significantly higher in normothermic groups (normothermia, normothermia + VPA) than in hypothermic groups (hypothermia, hypothermia + VPA). The hypothermia + VPA group showed significantly higher HSP70 mRNA expression than the hypothermia group. Similarly, at five hours after ROSC, HSP70 protein levels were significantly higher in normothermic groups than in hypothermic groups. HSP70 levels were significantly higher in the hypothermia + VPA group than in the hypothermia group. Only the hypothermia + VPA group showed significantly attenuated cleaved caspase-9 levels than the normothermia group. Hypothermia can attenuate the expression of HSP70 at transcriptional level. However, VPA administration can induce hyperacetylation of histone H3, leading to epigenetic transcriptional activation of HSP70 even in a hypothermic status. Combining VPA treatment with hypothermia may compensate for reduced activation of HSP70-mediated anti-apoptotic pathway.
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Wang, Gerald J., Holly Y. Deng, Carolina M. Maier, Guo Hua Sun, and Midori A. Yenari. "ICAM-1 Expression, Neutrophil & Monocyte Infiltration and Microglia Activation Reduced by Mild Hypothermia in a Rat Model of Transient Focal Cerebral Ischemia." Stroke 32, suppl_1 (January 2001): 354. http://dx.doi.org/10.1161/str.32.suppl_1.354-b.

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P84 BACKGROUND: Inflammation potentiates ischemic injury especially with reperfusion, while mild hypothermia is an effective neuroprotectant. We studied whether mild hypothermia’s protective effect may be due to blunting the inflammatory response. METHODS: We compared endothelial intracellular adhesion molecule (ICAM-1) expression, neutrophil & monocyte infiltration, and microglia activation under normothermic (38C n=24) and hypothermic (intraischemic brain cooling to 33C for 2h n=24) conditions 1,3, and 7 days following transient (2h) focal cerebral ischemia in rats. ICAM-1, ED-1 (to detect cells of monocyte lineage including activated microglia) and myeloperoxidase (MPO, to identify neutrophils) were detected using immunohistochemistry on brain sections. We measured cell densities of ICAM-1, ED-1, and MPO in the peri-infarct region. Infarct size was also measured from histology derived sizes of the ipsilateral hemisphere. RESULTS: Mild hypothermia reduced infarct size 1–7 days after stroke onset. 1d: 38C: 28±12%, 33C 8±6%; 3d: 38C: 39±23%, 33C: 11±11%; 7d: 38C: 37.3±5.8% vs 33C: 19.4±5.7% (p<0.05). The number of ICAM-1 positive vessels per high power field (HPF) decreased under hypothermia 1–7 days later. 1d: 38C: 35.8±1.7 vs 33C: 24.4±1.4 (p<0.01); 3d: 38C: 36.6±5.0 vs 33C: 23.5 1.3 (p=0.07); 7d: 38C: 69.9±2.7, 33C: 43±5.2 (p<0.001). In addition, neutrophil density (cells/12 HPF) decreased under hypothermic conditions at 1 and 3 days. 1d: 38C: 48±3.0 vs 33C: 1.3±0.6 (p<0.001), 3d: 38C: 75±3.5 vs 33C: 20.3±8.1 (p<0.001). Monocyte and microglial density (cells/HPF) was decreased by mild hypothermia at 3 and 7, but not 1 day. 1d: 38C: 17.5±0.9, 33C: 16.6±0.8, NS; 3d: 38C: 45.5±1.7, 33C: 19.2±0.9, (p<0.0001); 7d: 38C: 75.0 ±2.6, 33C: 24.8±3.0, (p<0.0001). CONCLUSIONS: Mild hypothermia reduces adhesion molecule expression, acute (neutrophil) and subacute (monocyte) leukocyte infiltration and microglial activation. These changes are present even days after hypothermic treatment, and suggest that hypothermia significantly attenuates the inflammatory response.
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Musacchia, X. J. "Endocrine regulation of carbohydrate metabolism in hypometabolic animals." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 167–72. http://dx.doi.org/10.1139/z88-023.

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Experimental hypothermia and natural hibernation are two forms of hypometabolism with recognized physiological changes, including depression of endocrine and metabolic functions. To better understand functional changes, helox (i.e., helium and oxygen (80:20) mixtures) and low ambient temperatures have been used to induce hypothermia in hamsters and rats. Both clinical and biological survival, i.e., survival without recovery and survival with recovery from hypothermia, respectively, are related to depth and length of hypothermia. In the rat, body temperatures of 15 °C for periods greater than 6–10 h greatly restrict biological survival. The role of glucocorticoids in enhancing thermogenic capacity of rats was assessed using triamcinalone acetonide. In the hamster, treatment with cortisone acetate prolonged both clinical and biological survival. Hypothermic hamsters continue utilizing circulating glucose until they become hypoglycemic and die. Hypothermic rats do not utilize glucose and respond with a significant hypoinsulinema. The role of endocrines in the regulation of carbohydrate homeostasis and metabolism differs in hibernation and hypothermia. Glucocorticoids influence the hypothermic response in both species, specifically by prolonging induction of hypothermia in rats and by prolonging survival in hypothermic hamsters.
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Shimada, S. G., J. T. Stitt, and P. Angelogianni. "Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2618–22. http://dx.doi.org/10.1152/jappl.1990.68.6.2618.

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Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.
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Paal, Peter, Mathieu Pasquier, Tomasz Darocha, Raimund Lechner, Sylweriusz Kosinski, Bernd Wallner, Ken Zafren, and Hermann Brugger. "Accidental Hypothermia: 2021 Update." International Journal of Environmental Research and Public Health 19, no. 1 (January 3, 2022): 501. http://dx.doi.org/10.3390/ijerph19010501.

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Accidental hypothermia is an unintentional drop of core temperature below 35 °C. Annually, thousands die of primary hypothermia and an unknown number die of secondary hypothermia worldwide. Hypothermia can be expected in emergency patients in the prehospital phase. Injured and intoxicated patients cool quickly even in subtropical regions. Preventive measures are important to avoid hypothermia or cooling in ill or injured patients. Diagnosis and assessment of the risk of cardiac arrest are based on clinical signs and core temperature measurement when available. Hypothermic patients with risk factors for imminent cardiac arrest (temperature < 30 °C in young and healthy patients and <32 °C in elderly persons, or patients with multiple comorbidities), ventricular dysrhythmias, or systolic blood pressure < 90 mmHg) and hypothermic patients who are already in cardiac arrest, should be transferred directly to an extracorporeal life support (ECLS) centre. If a hypothermic patient arrests, continuous cardiopulmonary resuscitation (CPR) should be performed. In hypothermic patients, the chances of survival and good neurological outcome are higher than for normothermic patients for witnessed, unwitnessed and asystolic cardiac arrest. Mechanical CPR devices should be used for prolonged rescue, if available. In severely hypothermic patients in cardiac arrest, if continuous or mechanical CPR is not possible, intermittent CPR should be used. Rewarming can be accomplished by passive and active techniques. Most often, passive and active external techniques are used. Only in patients with refractory hypothermia or cardiac arrest are internal rewarming techniques required. ECLS rewarming should be performed with extracorporeal membrane oxygenation (ECMO). A post-resuscitation care bundle should complement treatment.
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Naseri Alavi, Seyed Ahmd, Mohammad Amin Habibi, Alireza Majdi, Bardia Hajikarimloo, Farhang Rashidi, Sahar Fathi Tavani, Poriya Minaee, Seyed Mohammad Eazi, and Andrew J. Kobets. "Investigating the Safety and Efficacy of Therapeutic Hypothermia in Pediatric Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis." Children 11, no. 6 (June 7, 2024): 701. http://dx.doi.org/10.3390/children11060701.

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Background: Prior guidelines recommended maintaining normothermia following traumatic brain injury (TBI), but recent studies suggest therapeutic hypothermia as a viable option in pediatric cases. However, some others demonstrated a higher mortality rate. Hence, the impact of hypothermia on neurological symptoms and overall survival remains contentious. Methods: We conducted a systematic review and meta-analysis to evaluate the effects of hypothermia on neurological outcomes in pediatric TBI patients. The PubMed/Medline, Scopus, and Web of Science databases were searched until 1 January 2024 and data were analyzed using appropriate statistical methods. Results: A total of eight studies, comprising nine reports, were included in this analysis. Our meta-analysis did not reveal significant differences in mortality (RR = 1.58; 95% CI = 0.89–2.82, p = 0.055), infection (RR = 0.95: 95% CI = 0.79–1.1, p = 0.6), arrhythmia (RR = 2.85: 95% CI = 0.88–9.2, p = 0.08), hypotension (RR = 1.54: 95% CI = 0.91–2.6, p = 0.10), intracranial pressure (SMD = 5.07: 95% CI = −4.6–14.8, p = 0.30), hospital length of stay (SMD = 0.10; 95% CI = −0.13–0.3, p = 0.39), pediatric intensive care unit length of stay (SMD = 0.04; 95% CI = −0.19–0.28, p = 0.71), hemorrhage (RR = 0.86; 95% CI = 0.34–2.13, p = 0.75), cerebral perfusion pressure (SMD = 0.158: 95% CI = 0.11–0.13, p = 0.172), prothrombin time (SMD = 0.425; 95% CI = −0.037–0.886, p = 0.07), and partial thromboplastin time (SMD = 0.386; 95% CI = −0.074–0.847, p = 0.10) between the hypothermic and non-hypothermic groups. However, the heart rate was significantly lower in the hypothermic group (−1.523 SMD = −1.523: 95% CI = −1.81–−1.22 p < 0.001). Conclusions: Our findings challenge the effectiveness of therapeutic hypothermia in pediatric TBI cases. Despite expectations, it did not significantly improve key clinical outcomes. This prompts a critical re-evaluation of hypothermia’s role as a standard intervention in pediatric TBI treatment.
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Dissertations / Theses on the topic "Hypothermia"

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Léon, Karelle. "L'hypothermie modérée induite chez un modèle murin : une solution thérapeutique au sepsis ?" Thesis, Brest, 2012. http://www.theses.fr/2012BRES0030.

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Le sepsis, état pathologique lié à une réaction inflammatoire systémique suite à une infection, est lapremière cause de mortalité dans les unités de réanimation médicale et de soins intensifs hospitaliers.Parmi les pistes thérapeutiques envisagées, l’hypothermie est un bon candidat. En effet, l’hypothermiemodérée induite augmente la durée de survie de rats septiques. Ce travail avait pour objectifd’apporter des éléments permettant de comprendre et d’identifier les mécanismes responsables decet effet bénéfique. Pour cela, différentes fonctions couramment affectées lors du sepsis(inflammation, stress oxydant, défaillance rénale, capacités de transport de l’oxygène par le sang etéquilibre acide-base) ont été étudiées sur des rats septiques en hypothermie modérée (34°C). Lesrésultats obtenus révèlent que l’hypothermie modérée ralentit de manière significative la production decytokines pro-inflammatoires et tend à exercer une diminution de la production radicalaire systémiquechez les rats septiques. L’apparition de l’acidose métabolique et la défaillance rénale sont égalementretardées. Enfin, alors que le sepsis en normothermie conduit à une diminution de la coopérativité etde l’affinité de l’hémoglobine pour l’oxygène, synonymes d’une adaptation face à des modificationspotentiellement délétères, en hypothermie modérée, ces paramètres ne sont pas modifiés. Cesrésultats concourent à penser que l’hypothermie modérée en ralentissant l’évolution du sepsis permetd’augmenter la durée de survie des rats septiques. Ainsi, l’hypothermie pourrait constituer une pistepour traiter les patients atteints de sepsis sévère dans le but de temporiser l’inflammation et decontrôler l’agression retardant ainsi les défaillances d’organes
Despite numerous studies over the past twenty years, sepsis, a pathologic state related to a systemicinflammatory response following infection, remains the main cause of death in intensive care units.Among the therapeutic approaches proposed, hypothermia is a good candidate. Indeed, mild inducedhypothermia increased the survival duration of septic rats. This work aimed to provide elements tounderstand and identify the mechanisms responsible for this beneficial effect. Consequently, variousfunctions commonly affected during sepsis (inflammation, oxidative stress, renal failure, oxygen bloodcapacity and acid-base balance) were studied on septic rats maintained in mild induced hypothermia(34°C). The results showed that mild hypothermia significantly slows the cytokine proinflammatoryproduction and tends to exert a decrease in the radical systemic production of septic rats. Theappearance of metabolic acidosis and renal failure are also delayed. Finally, while in normothermiasepsis led to a decrease in the cooperativity and oxygen haemoglobin affinity, synonymous of anadaptation when faced with potential deleterious changes, in mild hypothermia, these parameters arenot modified. These results suggest that by reducing the development of sepsis, mild inducedhypothermia increases the survival duration of septic rats. Thus, hypothermia may be an option fortreating patients with severe sepsis by stalling inflammation and controlling aggression, therebydelaying organ failure
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Wladis, Andreas. "Hypothermia and trauma /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4574-8/.

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Islam, Shahed. "Therapeutic hypothermia in cardiovascular disease." Thesis, Anglia Ruskin University, 2017. http://arro.anglia.ac.uk/704083/.

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Introduction: Historical trials demonstrated clinical benefit of therapeutic hypothermia (TH) in unconscious cardiac arrest survivors. However, recent research raised important unanswered questions about this concept. Cardiac arrest associated mortality and morbidity including psychological trauma for survivors and caregivers remain alarmingly high, warranting further research in this field. TH has also been shown to offer additional protection against reperfusion injury in experimental models of myocardial ischaemia. However, co-administration of TH in conscious patients undergoing treatment for acute myocardial infarction (AMI) is potentially challenging. Methodology: (i) Rhinochill®, a novel intranasal cooling device is compared to Blanketrol for TH induction in unconscious cardiac arrest survivors, investigating efficacy and clinical outcome at hospital discharge. (ii) The emotional burden of cardiac arrest in patients and their caregivers is documented and the impact of simple interventions on quality of life is assessed. (iii) The feasibility of co-administration of TH in conscious patients undergoing emergency treatment of AMI is investigated. Results: (i) Rhinochill® is found to be more efficient in TH induction when measured from the tympanic membrane. However, Rhinochill® did not offer any superior clinical benefit. (ii) Simple psychological interventions are shown to improve quality of life in cardiac arrest survivors. (iii) Co-administration of endovascular cooling is shown to be feasible in conscious patients undergoing AMI treatment with minimum disruption to patient care. Discussion: Delays in TH administration may offset any potential benefit that it can offer in neuroprotection and therefore, earlier targeted brain cooling with more efficient portable devices is worth investigating. Improving quality of life of cardiac arrest survivors has been shown to be cost effective and therefore, investing in resources to better identify and help those at risk is justified. Delivery of TH in conscious heart attack patients is feasible and safe but more efficient endovascular cooling devices are required and these will need to be assessed in larger trials to assess the effect on clinical outcomes.
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Islam, Shahed. "Therapeutic hypothermia in cardiovascular disease." Thesis, Anglia Ruskin University, 2017. https://arro.anglia.ac.uk/id/eprint/704083/1/Islam_2017.pdf.

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Introduction: Historical trials demonstrated clinical benefit of therapeutic hypothermia (TH) in unconscious cardiac arrest survivors. However, recent research raised important unanswered questions about this concept. Cardiac arrest associated mortality and morbidity including psychological trauma for survivors and caregivers remain alarmingly high, warranting further research in this field. TH has also been shown to offer additional protection against reperfusion injury in experimental models of myocardial ischaemia. However, co-administration of TH in conscious patients undergoing treatment for acute myocardial infarction (AMI) is potentially challenging. Methodology: (i) Rhinochill®, a novel intranasal cooling device is compared to Blanketrol for TH induction in unconscious cardiac arrest survivors, investigating efficacy and clinical outcome at hospital discharge. (ii) The emotional burden of cardiac arrest in patients and their caregivers is documented and the impact of simple interventions on quality of life is assessed. (iii) The feasibility of co-administration of TH in conscious patients undergoing emergency treatment of AMI is investigated. Results: (i) Rhinochill® is found to be more efficient in TH induction when measured from the tympanic membrane. However, Rhinochill® did not offer any superior clinical benefit. (ii) Simple psychological interventions are shown to improve quality of life in cardiac arrest survivors. (iii) Co-administration of endovascular cooling is shown to be feasible in conscious patients undergoing AMI treatment with minimum disruption to patient care. Discussion: Delays in TH administration may offset any potential benefit that it can offer in neuroprotection and therefore, earlier targeted brain cooling with more efficient portable devices is worth investigating. Improving quality of life of cardiac arrest survivors has been shown to be cost effective and therefore, investing in resources to better identify and help those at risk is justified. Delivery of TH in conscious heart attack patients is feasible and safe but more efficient endovascular cooling devices are required and these will need to be assessed in larger trials to assess the effect on clinical outcomes.
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Covaciu, Lucian. "Intranasal Cooling for Cerebral Hypothermia Treatment." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-134278.

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The controlled lowering of core body temperature to 32°C to 34°C is defined as therapeutic hypothermia (TH). Therapeutic hypothermia has been shown to improve neurological outcome and survival in unconscious patients successfully resuscitated after cardiac arrest. Brain temperature is important for cerebral protection therefore methods for primarily cooling the brain have also been explored. This thesis focuses on the likelihood that intranasal cooling can induce, maintain and control cerebral hypothermia. The method uses bilaterally introduced intranasal balloons circulated with cold saline. Selective brain cooling induced with this method was effectively accomplished in pigs with normal circulation while no major disturbances in systemic circulation or physiological variables were recorded. The temperature gradients between brain and body could be maintained for at least six hours. Intranasal balloon catheters were used for therapeutic hypothermia initiation and maintenance during and after successful resuscitation in pigs. Temperature reduction was also obtained by combined intranasal cooling and intravenous ice-cold fluids with possible additional benefits in terms of physiologic stability after cardiac arrest. Rewarming was possible via the intranasal balloons. In these studies brain temperature was recorded invasively by temperature probes inserted in the brain. The fast changes in pig’s brain temperature could also be tracked by a non-invasive method. High-spatial resolution magnetic resonance spectroscopic imaging (MRSI) without internal reference showed a good association with direct invasive temperature monitoring. In addition the mapping of temperature changes during brain cooling was also possible. In awake and unsedated volunteers subjected to intranasal cooling brain temperature changes were followed by two MR techniques. Brain cooling was shown by the previously calibrated high-spatial resolution MRSI and by the phase-mapping method. Intranasal cooling reduced body temperature slightly. The volunteers remained alert during cooling, the physiological parameters stable, and no shivering was reported.
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Finiels, Amber. "Therapeutic hypothermia to prevent neurological deficits." Honors in the Major Thesis, University of Central Florida, 2010. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/1404.

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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.
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Bashir, Shazma. "Mechanism of Paracetamol (acetaminophen) induced hypothermia." Thesis, University of East London, 2018. http://roar.uel.ac.uk/7308/.

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Paracetamol is a potent analgesic and antipyretic with limited side effects compared to the nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates. Worldwide paracetamol is commonly used to treat pain and fever in both children and adults. Although, this drug has been in clinical use for more than a century, the mechanisms of action are not fully understood. Historically some of the actions of paracetamol were attributed to the inhibition of central cyclooxygenase (COX-1 and COX-2) enzymes however given the weak inhibitory effects on COX-1 and COX-2 enzymes, alternative targets have been suggested including a possible novel COX-3. The inhibition of COX-2 is accepted as the mechanism by which paracetamol reduces core temperature (Tc) in febrile animals. However, in non-febrile animals where COX-2 is not induced, paracetamol has also been shown to cause hypothermia by a mechanism that is not fully understood. Both the reduction of pyresis and induction of hypothermia can only occur when peripheral metabolic rate decreases and/or heat loss increases. In terms of antipyresis and hypothermia, the inhibition of lipolysis, fatty acid oxidation and mitochondria function are obvious alternative targets. Studies were undertaken to identify and characterise the putative COX-3 at protein and mRNA level using western blot analysis and reverse transcription polymerase chain reaction (RT-PCR) in mouse brain endothelial cells (b.End3) and whole brain tissues isolated from male C57BL/6 mice. Additional studies were also undertaken to assess if the hypothermic properties of paracetamol could be attributed to direct inhibition of thermogenic pathways in both 3T3-L1 adipocytes and primary brown adipocytes isolated from male Wistar rats. Adipocytes and isolated mitochondria were exposed to paracetamol and lipolysis, fatty acid oxidation (FAO), mitochondrial electron transport chain (ETC), assessed by measuring oxygen consumption rate (OCR). In these studies no expression of the COX-3 protein could be detected in brain endothelial cells and homogenates and no evidence of a COX-3 was detected at mRNA level. However, paracetamol caused a significant decrease (upto 70%; P < 0.01, from control) in both basal and stimulated lipolysis at 1, 3 and 24 hours without affecting cell viability. Paracetamol (10 mM) and its metabolite N-acetyl-p-benzoquinone imine (NAPQI) at 50 μM also significantly (P < 0.01, from control), reduced endogenous and exogenous FAO by 50% and 70% respectively. NAPQI (50 μM) had limited effect on mitochondrial uncoupling. Finally, paracetamol and other antipyretic compounds also significantly reduced ETC activity (upto 90%; P < 0.01, from control). Both the maintenance of normal body temperature (Tb) and the induction of pyresis require increased mitochondrial ETC activity normally initiated centrally and driven peripherally by reduction of substrates such as fatty acids and glucose. The failure to identify the COX-3 protein and the direct inhibition of lipolysis, FAO and ETC activity indicate that antipyretic actions of paracetamol could partly be attributed to it actions on peripheral energy generation systems and provide new drug targets for reducing fever and chemically inducing hypothermia.
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Hutin, Alice. "Etude expérimentale de l’arrêt cardiaque réfractaire chez le porc : nouvelles approches thérapeutiques." Thesis, Paris Est, 2017. http://www.theses.fr/2017PESC0030/document.

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L’arrêt cardiaque (AC) extrahospitalier est un problème majeur de santé publique, malgré la mise en place d’une véritable « chaine de survie ». Les durées de réanimation sont souvent prolongées et aboutissent à des séquelles irréversibles avec un assombrissement dramatique du pronostic. Dans de nombreuses situations, l’AC ne parvient pas à être réanimé avec les soins courants, laissant apparaître un AC « réfractaire » qui nécessite une prise en charge thérapeutique avancée. L’objectif général de ce travail de thèse était d’évaluer de nouvelles approches expérimentales pour la prise en charge de l’AC réfractaire. Nous avons étudié deux stratégies expérimentales chez le porc, consistant à induire une hypothermie ultra-rapide par ventilation liquide ou à mettre en place une assistance circulatoire au cours d’un AC d’origine ischémique.Dans un premier travail, nous avons ainsi évalué la faisabilité d’une hypothermie thérapeutique ultra-rapide par ventilation liquidienne totale (VLT) chez le porc. Cette approche consiste à instiller des perfluorocarbones dans le poumon de façon à induire un refroidissement ultra-rapide. Le poumon est ainsi utilisé comme bio-échangeur thermique, tout en maintenant des échanges gazeux normaux. Dans des travaux préliminaires, le laboratoire a montré que la VLT permettait de réduire la température sanguine jusqu’à 32°C en moins de 10 minutes chez le lapin. Le but de notre étude était de déterminer si la VLT pouvait aussi permettre un refroidissement ultra-rapide chez le porc. L'effet de la VLT a ainsi été évalué dans un premier temps à cœur battant, puis à cœur arrêté sur un modèle d’arrêt cardiaque réfractaire bénéficiant d’une réanimation cardio-pulmonaire prolongée. Dans les conditions physiologiques « à cœur battant », la température de 34°C était atteinte en moins de 10 minutes dans tout l'organisme. Lors de la réanimation prolongée d’un AC réfractaire, le refroidissement corporel était également obtenu rapidement, en moins de 25 minutes, quel que soit le site de mesure de la température. La VLT n’altérait aucunement la qualité du massage cardiaque externe, suggérant un intérêt pour cette approche dans l’induction d‘une hypothermie intra-AC, dans une perspective d’augmentation de l’efficacité des défibrillations ou de préservation d’organe.Dans un deuxième travail, nous nous sommes intéressés à l’AC réfractaire compliquant un syndrome coronaire aigu, traité par assistance circulatoire extracorporelle. Notre but était d’évaluer l'importance de la revascularisation coronaire précoce dans cette situation chez le porc, c’est-à-dire son impact sur le statut hémodynamique et les chances de réanimation. Après anesthésie et instrumentation, les animaux ont ainsi été soumis à une occlusion coronaire, suivie d’un AC par fibrillation ventriculaire non traitée pendant 5 minutes. Ils ont ensuite bénéficié d’une réanimation cardio-pulmonaire de base puis d’une assistance circulatoire extracorporelle. Nous avons comparé les effets d’une revascularisation précoce à ceux d’une revascularisation tardive, c’est-à-dire d’une reperfusion 20 ou 120 min après le début de l'assistance circulatoire. La revascularisation coronaire précoce augmentait significativement les chances de reprise d’activité cardiaque spontanée, limitait l’état de choc, améliorait la perfusion cérébrale et limitait la taille d’infarctus. Cela montre bien l’importance d’une prise en charge rapide du syndrome coronarien en cas d’AC de cause cardiaque présumée, y compris dans une situation d’assistance circulatoire extracorporelle.En conclusion, nous avons montré que la VLT permettait d’induire un refroidissement ultra-rapide dans l’ensemble de l’organisme, tant à cœur battant que pendant une réanimation prolongée. Par ailleurs, la revascularisation précoce d’un AC réfractaire ischémique traité par assistance circulatoire extracorporelle permettait d’améliorer globalement les chances de réanimation et le statut hémodynamique
Out of hospital cardiac arrest (CA) is a major public health issue, despite the implementation of a “chain of survival”. Resuscitation durations are often extended with irreversible organ damage and poor outcome. Frequently, conventional care does not allow the return of spontaneous circulation, leading to a refractory CA, with the need for advanced therapeutic care. The general objective of this work was to evaluate new therapeutic strategies in the management of refractory cardiac arrest. We studied two experimental strategies in swine, involving ultrafast cooling with total liquid ventilation or extracorporeal cardiopulmonary resuscitation in a CA of ischemic origin.As a first step, we evaluated the feasibility of ultra-fast therapeutic hypothermia using total liquid ventilation (TLV) in swine. This approach involves perfluorocarbon instillation in the lungs to induce ultra-fast cooling. The lungs are thus used as a heat exchanger, while maintaining normal gas exchanges. In previous studies, the laboratory has shown that TLV could reduce blood temperature to 32°C in less than 10 minutes in rabbits. The objective of this study was to determine if TLV could lead to ultra-fast cooling in swine. We first studied the cooling capacity of hypothermic TLV in beating heart pigs, and then during ventricular fibrillation with prolonged chest compressions. In physiological conditions, in “beating heart” animals, the target temperature of 34°C was obtained in less than 10 min in the whole body. In prolonged resuscitation of refractory CA, whole body cooling was also rapidly obtained, within less than 25 min. TLV did not alter the hemodynamic effect of cardiac compressions, suggesting further use of this “intra-resuscitation” cooling in order to increase chances of defibrillation or for organ preservation for the purpose of organ donation.As a second step, we addressed the subject of ischemic refractory CA treated by extracorporeal cardiopulmonary resuscitation (ECPR). Our objective was to evaluate the importance of early coronary reperfusion in this situation, i.e., it’s impact on hemodynamic status and chances of defibrillation. After anesthesia and surgical preparation, animals were submitted to a coronaryocclusion followed by 5 min of CA by ventricular fibrillation. Conventional cardiopulmonary resuscitation was then initiated and followed by extracorporeal cardiopulmonary resuscitation.We compared the effect of early versus late reperfusion, i.e., reperfusion after 20 or 120 min of ECPR. Early reperfusion significantly increased chances of return to spontaneous circulation with limited shock status, increased cerebral perfusion and decreased infarct size. This confirms the need for early treatment of acute coronary syndrome if cardiac cause of CA is suspected, even in the situation of ECPR.In conclusion, we have shown that TLV could provide ultra-fast whole body cooling, both in beating heart swine and during prolonged resuscitation. Secondly, early reperfusion in refractory ischemic CA treated by ECPR globally increases chances of return to spontaneous circulation and improves hemodynamic status
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Klock, Julia Cathy. "Rapid whole-body hypothermia : analysis and modeling /." View online ; access limited to URI, 2007. http://0-digitalcommons.uri.edu.helin.uri.edu/dissertations/AAI3276989.

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Collins, Michael. "Dysphagia in Encephalopathic Neonates Treated with Hypothermia." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/281173.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Objective: The purpose of this study is to determine the rate of dysphagia in neonates treated with targeted body temperature reduction as compared to neonates who have not been exposed to hypothermia. Methods: We performed a retrospective study of encephalopathic neonates who were treated with hypothermia and who underwent a modified barium swallow (MBS). For comparison, a group of neonates who had been evaluated with MBS but did not receive hypothermic therapy was identified. This group consisted of non-encephalopathic patients. MBS results were qualified as either normal or abnormal. Results: There was no statistically significant difference in the percentage of abnormal MBS results between the hypothermic and control groups (Fisher’s exact; P = 0.78). The odds ratio for abnormal MBS results in the hypothermia group relative to the control group was 1.2, with 95% confidence interval of 0.42 to 3.8. Significance: These data indicate that hypothermia does not seem to increase short term risk of dysphagia compared to the control group. There is no apparent association between hypothermia and dysphagia. This supports previous findings that hypothermia is a safe treatment for neural injuries in NICU patients.
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Books on the topic "Hypothermia"

1

Indriðason, Arnaldur. Hypothermia. New York: Minotaur Books, 2010.

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Indriðason, Arnaldur. Hypothermia. Rearsby, Leicester: W.F. Howes, 2009.

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Hayashi, Nariyuki, ed. Brain Hypothermia. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66882-4.

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Tisherman, Samuel A., and Fritz Sterz, eds. Therapeutic Hypothermia. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/b107316.

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A, Mayer Stephan, and Sessler Daniel, eds. Therapeutic hypothermia. New York: Marcel Dekker, 2005.

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Hayashi, Nariyuki, and Dalton W. Dietrich. Brain Hypothermia Treatment. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7.

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Lee, McManus, ed. Hypothermia: The facts. London: Age Concern England, 1986.

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1952-, Dietrich D. W., ed. Brain hypothermia treatment. Tokyo: Springer-Verlag, 2004.

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Maier, Carolina M., and Gary K. Steinberg. Hypothermia and Cerebral Ischemia. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592596533.

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Aging, National Institute on, and National Institutes of Health (U. S.), eds. [Hypothermia and older adults]. [Washington, D.C.?]: National Institutes of Health, 2006.

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Book chapters on the topic "Hypothermia"

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Reuler, James B. "Hypothermia." In Geriatric Medicine, 579–84. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4757-2093-8_44.

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Dettmeyer, Reinhard B. "Hypothermia." In Forensic Histopathology, 207–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77997-3_8.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, David C. S. Roberts, Eileen M. Joyce, Jonathan P. Roiser, John H. Halpern, et al. "Hypothermia." In Encyclopedia of Psychopharmacology, 615. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_769.

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Ioan, Beatrice Gabriela. "Hypothermia." In Encyclopedia of Immigrant Health, 865–66. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5659-0_379.

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White, J. D. "Hypothermia." In Update in Intensive Care and Emergency Medicine, 31–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70309-6_6.

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Varelmann, Dirk J. "Hypothermia." In Anesthesiology, 29–32. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50141-3_4.

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Dettmeyer, Reinhard B. "Hypothermia." In Forensic Histopathology, 165–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-20659-7_8.

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El-Radhi, A. Sahib. "Hypothermia." In Clinical Manual of Fever in Children, 193–210. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92336-9_8.

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Davies, Eryl. "Hypothermia." In The Final FFICM Structured Oral Examination Study Guide, 190–91. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003243694-64.

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Payne-James, Jason, and Roger W. Byard. "Hypothermia." In Forensic and Legal Medicine, 390–95. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003138754-47.

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Conference papers on the topic "Hypothermia"

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K, Danno, Worku DT, Adjaho I, Ale F, Katuala Y, Mbuyi Y, and Evboumwam PE. "Incidence and contextual analysis of neonatal hypothermia at Garan Gamawa Maternal and Child Health Clinic in Kano State, Nigeria, 2022." In MSF Paediatric Days 2024. NYC: MSF-USA, 2024. http://dx.doi.org/10.57740/omknx6.

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BACKGROUND AND OBJECTIVES Hypothermia is a major risk factor for high neonatal mortality. In January, night-time temperatures in Kano State can drop below 20°C. We conducted a study to elucidate the incidence of neonatal hypothermia at Garan Gamawa maternal and child health (MCH) clinic in Kano City, with an aim to improve midwifery care and reduce hypothermia-related neonatal mortality. METHODS The data of neonates born in January 2022 were collected retrospectively in February 2022. Hypothermia was defined as “axillary temperature below 35.5°C” in accordance with MSF Essential Obstetric and Newborn Care guidelines, 2019. Statistical analysis was done using a one-sided test for binomial proportions. Qualitative data was garnered by non-participatory observation (NPO) in the delivery room and postnatal care (PNC) ward to observe the warm chain and the interactions between staff and mothers. Individual semi-structured in-depth interviews were also conducted with eight MCH staff. RESULTS Amongst the 206 newborns included, 55 (26.69%, Wilson confidence interval 21.13- 33.13%, p value < 0.00001) developed hypothermia. From the NPO, contributing factors to hypothermia included: absence of skin-to-skin at birth; a delay of 40 minutes between birth and baby being put to the breast for their first feed; constant draught of outside air into delivery room; absence of heating system in delivery room and PNC ward; and the need to go outside during transfer between the delivery room and PNC ward. In-depth interviews illustrated that midwives prioritised dressing the babies rather than encouraging Kangaroo Mother Care (KMC), and that the warm chain was prone to interruption during a complicated delivery and when there were multiple labouring mothers. Additionally, some midwives were not aware of the definition of neonatal hypothermia. CONCLUSIONS The proportion of hypothermic neonates was significant, and several contributing factors were identified. Recommendations include the installation of a door into the delivery room and appropriate heating systems in both the delivery room and PNC ward. Training of MCH staff is required to build knowledge and skills regarding the maintenance of the warm chain, and highlighting the importance of immediate skin-to-skin at birth and KMC, which have an important role in preventing hypothermia and must be encouraged.
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Collins, L., J. Wood, A. Faire, G. Kakade, S. Barrett, F. Patel, Deepa Panjwani, and S. Rao. "114 Hypothermia is preventable." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.114.

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Vasilkov, Valery G., Alexey I. Safronov, and Dmitriy V. Osinkin. "LOCAL ABDOMINAL HYPOTHERMIA APPARATUS." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.18.

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Isik, Hakan, I. Unal Sert, Nuri Yavru, and Novruz Allahverdi. "Microcontroller based hypothermia system." In the 2007 international conference. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1330598.1330628.

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Alleyne-Agard, D., C. Chao, D. J. Brown, Z. Khan, and M. Bachan. "Moderate Hypothermia Without Arrhythmias." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1736.

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Kattih, Z., J. Le, E. L. Altschul, and B. A. Mina. "Hypothermia, Rewarming, and Potassium Shifting: A Case of Accidental Hypothermia and Hyperkalemia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5175.

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Al-Shamari, M., R. Puttha, S. Yuen, D. Rees, C. Curson, S. Goldengay, G. Armstrong, and M. Panchal. "G9 Can introduction of a hypothermia bundle reduce hypothermia in the newborns?" In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.9.

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Companion, J., J. S. Heyman, J. R. Oleson, and M. Engler. "Ultrasonic Hypothermia Temperature Monitoring Technique." In IEEE 1986 Ultrasonics Symposium. IEEE, 1986. http://dx.doi.org/10.1109/ultsym.1986.198881.

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Macfarlane, KA, and LE Bruce. "G275(P) Hats for hypothermia." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.267.

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Jeganathan, Niranjan, Anthony Marinelli, Melvin Speisman, and Vemuri Murthy. "Therapeutic Hypothermia After Cardiac Arrest." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3166.

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Reports on the topic "Hypothermia"

1

Pozos, R. S., P. A. Iaizzo, and D. F. Danzl. Hypothermia. Fort Belvoir, VA: Defense Technical Information Center, July 1993. http://dx.doi.org/10.21236/ada378267.

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Gill, Ralph E. Devices for Emergency Hypothermia and Military Applications. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada419477.

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Armstrong, Lawrence E. What Should Athletes Know About Low Body Temperature (Hypothermia). Fort Belvoir, VA: Defense Technical Information Center, October 1989. http://dx.doi.org/10.21236/ada218316.

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Michelson, A. D., H. MacGregor, A. Kestin, M. R. Barnard, and M. J. Rohrer. Reversible Hypothermia-Induced Inhibition of Human Platelet Activation in Whole Blood in Vitro and in Vivo. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada360296.

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Matthew, Candace B., Ingrid V. Sils, and Amy M. Bastille. Flunarizine Attenuates Hypothermia/Rewarming-Induced Changes in Protein and Water Movement Across the Endothelium of Rats. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada414632.

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Park, Marcelo, and Ian Maia. The Extracorporeal Pulmonary Resuscitation Effect on Survival and Quality of Life in Refractory Cardiac Arrest Patients: A Systematic Review of the Literature with Metanalysis and Trial Sequential Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0011.

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Review question / Objective: Questions: Cumulative effects of the ECPR trials on the last reported quality of life (Cerebral performance category) (accomplishing in and/or out of hospital cardiac arrests). Cumulative effects of the ECPR trials on the last reported Survival. (accomplishing in and/or out of hospital cardiac arrests). Condition being studied: Inclusion criteria: Adult (> 18 years-old) patients; Refractory cardiac arrest (> 5 min); With or without hypothermia after resuscitation; Witness and assisted cardiac arrests; Any cardiac rhythm of cardiac arrest; Any mechanism of cardiac arrest; In-hospital and out-of-hospital cardiac arrestsExtracorporeal cardiopulmonary resuscitation cannulation in any place; Studies with a conventional cardiopulmonary resuscitation paired group (Randomized, propensity score paired and emulated studies).
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Wu, Jinze, Zengliang Wang, Yan Feng, and Chaoyang Zhang. Outcomes of therapeutic hypothermia combined with decompressive craniectomy for malignant middle cerebral artery infarction: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0075.

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Kumar, Matthew M. A Novel Method for Inducing Therapeutic Hypothermia in a Swine Model of Blast-Induced Traumatic Brain Injury with Associated Hemorrhagic Shock. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada560801.

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Miller, Harvey I. Metabolic Changes and Hemodynamic Dysfunction Following Hypothermic Chock. Fort Belvoir, VA: Defense Technical Information Center, March 1992. http://dx.doi.org/10.21236/ada249748.

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Miller, Harvey I. Metabolic Changes and Hemodynamic Dysfunction Following Hypothermic Shock. Fort Belvoir, VA: Defense Technical Information Center, June 1993. http://dx.doi.org/10.21236/ada269780.

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