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Journal articles on the topic 'Hypothermia'
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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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Nguyen, Hoang P., Jonathan G. Zaroff, Emine O. Bayman, Adrian W. Gelb, Michael M. Todd, and Bradley J. Hindman. "Perioperative Hypothermia (33°C) Does Not Increase the Occurrence of Cardiovascular Events in Patients Undergoing Cerebral Aneurysm Surgery." Anesthesiology 113, no. 2 (August 1, 2010): 327–42. http://dx.doi.org/10.1097/aln.0b013e3181dfd4f7.
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Background Perioperative hypothermia has been reported to increase the occurrence of cardiovascular complications. By increasing the activity of sympathetic nervous system, perioperative hypothermia also has the potential to increase cardiac injury and dysfunction associated with subarachnoid hemorrhage. Methods The Intraoperative Hypothermia for Aneurysm Surgery Trial randomized patients undergoing cerebral aneurysm surgery to intraoperative hypothermia (n = 499, 33.3 degrees +/- 0.8 degrees C) or normothermia (n = 501, 36.7 degrees +/- 0.5 degrees C). Cardiovascular events (hypotension, arrhythmias, vasopressor use, myocardial infarction, and others) were prospectively followed until 3-month follow-up and were compared in hypothermic and normothermic patients. A subset of 62 patients (hypothermia, n = 33; normothermia, n = 29) also had preoperative and postoperative (within 24 h) measurement of cardiac troponin-I and echocardiography to explore the association between perioperative hypothermia and subarachnoid hemorrhage-associated myocardial injury and left ventricular function. Results There was no difference between hypothermic and normothermic patients in the occurrence of any single cardiovascular event or in composite cardiovascular events. There was no difference in mortality (6%) between groups, and there was only a single primary cardiovascular death (normothermia). There was no difference between hypothermic and normothermic patients in postoperative versus preoperative left ventricular regional wall motion or ejection fraction. Compared with preoperative values, hypothermic patients had no postoperative increase in cardiac troponin-I (median change 0.00 microg/l), whereas normothermic patients had a small postoperative increase (median change + 0.01 microg/l, P = 0.038). Conclusion In patients undergoing cerebral aneurysm surgery, perioperative hypothermia was not associated with an increased occurrence of cardiovascular events.
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Tessema, Tegenu, Tilahun Ferede Asena, Meseret Mosissa Alemayehu, and Asmare Mekonnen Wube. "Risk factors for neonatal hypothermia at Arba Minch General Hospital, Ethiopia." PLOS ONE 17, no. 12 (December 22, 2022): e0267868. http://dx.doi.org/10.1371/journal.pone.0267868.
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Background The first few minutes after birth are the most dangerous for the survival of an infant. Babies in neonatal intensive care units are either under heated or overheated, and hypothermic infants remain hypothermic or develop a fever. As a result, special attention must be paid to monitoring and maintaining the time of recovery from hypothermia states. Despite numerous studies, only a few have examined the transition from neonatal hypothermia and associated risk factors in depth. Method A retrospective observational study was conducted to track axillary temperatures taken at the time of neonatal intensive care unit admission, which were then tracked every 30 minutes until the newborn’s temperature stabilized. All hypothermic neonates admitted to the neonatal intensive care unit between January 2018 and December 2020 was included in the study. Temperature data were available at birth and within the first three hours of admission for 391 eligible hypothermic neonates. The effect of factors on the transition rate in different states of hypothermia was estimated using a multi-state Markov model. Result The likelihood of progressing from mild to severe hypothermia was 5%, while the likelihood of progressing to normal was 34%. The average time spent in a severe hypothermia state was 48, 35, and 24 minutes for three different levels of birth weight, and 53, 41, and 31 minutes for low, moderate, and normal Apgar scores, respectively. Furthermore, the mean sojourn time in a severe hypothermia state was 48, 39, and 31 minutes for three different levels of high, normal, and low pulse rate, respectively. Conclusion For hypothermic survivors within the first three hours of life, very low birth weight, low Apgar, and high pulse rate had the strongest association with hypothermia and took the longest time to improve/recover. As a result, there is an urgent need to train all levels of staff dealing with maintaining the time of recovery from neonatal hypothermia.
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Miranda, David, Rebecca Maine, Mackenzie Cook, Scott Brakenridge, Lyle Moldawer, Saman Arbabi, Grant O'Keefe, et al. "Chronic critical illness after hypothermia in trauma patients." Trauma Surgery & Acute Care Open 6, no. 1 (July 2021): e000747. http://dx.doi.org/10.1136/tsaco-2021-000747.
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ObjectivesChronic critical illness (CCI) is a phenotype that occurs frequently in patients with severe injury. Previous work has suggested that inflammatory changes leading to CCI occur early following injury. However, the modifiable factors associated with CCI are unknown. We hypothesized that hypothermia, an early modifiable factor, is associated with CCI.MethodsTo determine the association of hypothermia and CCI, a secondary analysis of the Inflammation and Host Response to Injury database was performed, and subsequently validated on a similar cohort of patients from a single level 1 trauma center from January 2015 to December 2019. Hypothermia was defined as initial body temperature ≤34.5°C. CCI was defined as death or sustained multiorgan failure ≥14 days after injury. Data were analyzed using univariable analyses with Student’s t-test and Pearson’s χ2 test, and logistic regression. An arrayed genomic analysis of the transcriptome of circulating immune cells was performed in these patients.ResultsOf the initial 1675 patients, 254 had hypothermia and 1421 did not. On univariable analysis, 120/254 (47.2%) of patients with hypothermia had CCI, compared with 520/1421 (36.6%) without hypothermia who had CCI, p<0.001. On multivariable logistic regression, hypothermia was independently associated with CCI, OR 1.61 (95% CI 1.17 to 2.21) but not mortality. Subsequent validation in 1264 patients of which 172 (13.6%) were hypothermic, verified that hypothermia was independently associated with CCI on multivariable logistic regression, OR 1.84 (95% CI 1.21 to 2.41). Transcriptomic analysis in hypothermic and non-hypothermic patients revealed unique cellular-specific genomic changes to only circulating monocytes, without any distinct effect on neutrophils or lymphocytes.ConclusionsHypothermia is associated with the development of CCI in severely injured patients. There are transcriptomic changes which indicate that the changes induced by hypothermia may be associated with persistent CCI. Thus, early reversal of hypothermia following injury may prevent the CCI.Level of evidenceIII.
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Yuan, Hui-Bih, Yueming Huang, Shuqiu Zheng, and Zhiyi Zuo. "Hypothermic Preconditioning Increases Survival of Purkinje Neurons in Rat Cerebellar Slices after an In Vitro Simulated Ischemia." Anesthesiology 100, no. 2 (February 1, 2004): 331–37. http://dx.doi.org/10.1097/00000542-200402000-00023.
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Background A period of hypothermia before ischemia (hypothermic preconditioning) induces a delayed phase of ischemic tolerance in rat brain. However, whether hypothermic preconditioning induces an acute phase (within a few hours after the hypothermia) of ischemic tolerance remains unknown. This study was designed to determine the time window of the hypothermic preconditioning-induced acute phase of neuroprotection, which is useful information for situations during surgery with anticipated ischemic episodes, and its involved mechanisms. Methods Survival of Purkinje cells in rat cerebellar slices was evaluated after a 20-min oxygen-glucose deprivation (OGD, in vitro simulated ischemia) followed by a 4-h recovery. Mild hypothermia (33 degrees C) for 20 min was applied at various times before the OGD. Results The hypothermia applied immediately to 3 h before the OGD equally effectively reduced OGD-induced Purkinje cell death/injury. Glibenclamide, a selective KATP channel blocker; 8-cyclopentyl-1,3-dipropylxanthine, a selective adenosine A1 receptor antagonist; and farnesyl protein transferase inhibitor III, a selective inhibitor to reduce Ras farnesylation, abolished hypothermic preconditioning-induced neuroprotection when applied during the hypothermia. OGD increased the expression of high-mobility group I(Y) proteins, which are nuclear transcription factors to enhance the expression of putatively damaging proteins such as cyclooxygenase-2, in cerebellar slices. This increase was attenuated by hypothermic preconditioning. Conclusions Hypothermic preconditioning induces an acute phase of neuroprotection. This neuroprotection depends on activation of the signaling molecules, adenosine A1 receptors, KATP channels, and Ras. Inhibition of putatively damaging proteins via the effects of hypothermic preconditioning on high-mobility group I(Y) expression may also be involved in hypothermic preconditioning-induced neuroprotection.
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Krause, Kevin R., Greg A. Howells, Chad L. Buhs, Diego A. Hernandez, Holly Bair, Michelle Schuster, and Phillip J. Bendick. "Hypothermia-Induced Coagulopathy during Hemorrhagic Shock." American Surgeon 66, no. 4 (April 2000): 348–54. http://dx.doi.org/10.1177/000313480006600406.
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A porcine model of hemorrhagic shock was used to study the effect of hypothermia on hemodynamic, metabolic, and coagulation parameters. The model was designed to simulate the events of severe blunt injury with hemorrhage occurring initially, to a systolic blood pressure of 30 mm Hg, followed by simultaneous hemorrhage and crystalloid volume replacement, followed by cessation of hemorrhage and blood replacement. Half of the animals were rendered hypothermic by external application of ice, and half remained normothermic. There was seven pigs in each group. Two deaths occurred in each during the hemorrhage phase. The hypothermic pigs demonstrated larger reduction in cardiac output than normothermic pigs. Volume replacement in the normothermic group restored cardiac output to baseline values. In the hypothermic group, cardiac output remained depressed despite volume replacement. Prothrombin times and partial thromboplastin times showed significantly more prolongation in the hypothermic group. Furthermore, this was not corrected by replacement of shed blood in the hypothermic group, as was seen in the normothermic group. We conclude that when shock and hypothermia occur together, their deleterious effect on hemodynamic and coagulation parameters are additive. The effects of hypothermia persist despite the arrest of hemorrhage and volume replacement. Thus, it is necessary to aggressively address both shock and hypothermia when they occur simultaneously.
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Kanodia, Piush, R. Bhandari, N. Bhatta, and S. Yadav. "Evaluation of Hypothermia in Sick Neonates as Predictor of Fatality at a Tertiary Care Center of Eastern Nepal." Journal of Nepalgunj Medical College 14, no. 2 (October 31, 2018): 8–11. http://dx.doi.org/10.3126/jngmc.v14i2.21527.
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Introduction: Hypothermia is a common and frequent problem in newborns. It has larger impact in outcome related to management of sick infants.Objective: To correlate the severity of hypothermia in sick extramural neonates with fatality and physiological derangements.Materials and Methods: This prospective observational study was carried out at Neonatology unit of Pediatric department of B. P. Koirala Institute of Health Sciences (BPKIHS) Dharan. Total 200 extramural hypothermic neonates were transferred to BPKIHS from June 2015 to June 2016. Neonates weighing more than 1000 g, with abdominal skin temperature less than 36.5°C at admission were included in the study.. Clinical features and associated features were recorded at the time of admission. Oxygen saturation was recorded by a pulse oximeter.Results: Fatality was observed to be 39.3% in mildly hypothermic babies, 51.6% in moderately hypothermic babies and 80% in severely hypothermic babies. However, the presence of associated illness (birth asphyxia, neonatal sepsis and respiratory distress), physiological derangements (hypoxia, hypoglycemia and shock) and weight less than 2000 g were associated with more than 50% fatality even in mildly hypothermic babies. When moderate hypothermia was associated with hypoxia or shock, the fatality was 83.3% and 90.9%, respectively. Similarly, mild hypothermia with hypoglycemia was associated with 71.4% fatality.Conclusion: The presence of associated illness (birth asphyxia, neonatal sepsis and respiratory distress), physiological derangements (hypoxia, hypoglycemia and shock) and weight less than 2000 g should be considered adverse factors in hypothermic neonates. Their presence should classify hypothermia in the next higher category of severity in WHO classification. JNGMC Vol. 14 No. 2 December 2016, page: 8-11
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Fonseca, Monique T., Abner C. Rodrigues, Luana C. Cezar, Andre Fujita, Francisco G. Soriano, and Alexandre A. Steiner. "Spontaneous hypothermia in human sepsis is a transient, self-limiting, and nonterminal response." Journal of Applied Physiology 120, no. 12 (June 15, 2016): 1394–401. http://dx.doi.org/10.1152/japplphysiol.00004.2016.
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Hypothermia in sepsis is generally perceived as something dysregulated and progressive although there has been no assessment on the natural course of this phenomenon in humans. This was the first study on the dynamics of hypothermia in septic patients not subjected to active rewarming, and the results were surprising. A sample of 50 subjects presenting with spontaneous hypothermia during sepsis was drawn from the 2005-2012 database of an academic hospital. Hypothermia was defined as body temperature below 36.0°C for longer than 2 h, with at least one reading of 35.5°C or less. The patients presented with 138 episodes of hypothermia, 21 at the time of the sepsis diagnosis and 117 with a later onset. However, hypothermia was uncommon in the final 12 h of life of the patients that succumbed. The majority (97.1%) of the hypothermic episodes were transient and self-limited; the median recovery time was 6 h; body temperature rarely fell below 34.0°C. Bidirectional oscillations in body temperature were evident in the course of hypothermia. Nearly half of the hypothermic episodes had onset in the absence of shock or respiratory distress, and the incidence of hypothermia was not increased during either of these conditions. Usage of antipyretic drugs, sedatives, neuroleptics, or other medications did not predict the onset of hypothermia. In conclusion, hypothermia appears to be a predominantly transient, self-limiting, and nonterminal phenomenon that is inherent to human sepsis. These characteristics resemble those of the regulated hypothermia shown to replace fever in animal models of severe systemic inflammation.
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Shevelev, Oleg A., Marina V. Petrova, Shavkat Kh Saidov, Nadezhda A. Khodorovich, and Pranil Pradkhan. "Neuroprotection Mechanisms in Cerebral Hypothermia (Review)." General Reanimatology 15, no. 6 (December 24, 2019): 94–114. http://dx.doi.org/10.15360/1813-9779-2019-6-94-114.
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The review focuses on the neuroprotective mechanisms of therapeutic hypothermia from the standpoint of metabolic depression and genomic reprogramming of neurons that develop when brain temperature decreases.The concept of hypothermic pre-conditioning based on the development of typical nonspecific reactions for the formation of the cytoprotective phenotype of neurons due to potentially dangerous stimuli, such as ischemia, reperfusion, and hypothermia, was used to explain the effects of low temperatures. The data confirming the role of therapeutic cerebral hypothermia as a technique of selective brain exposure to mild cold for the neuroprotection and correction of temperature balance disorders are shown.The approach to therapeutic hypothermia as a hypothermic pre-conditioning allows to significantly expand the scope of its use in various procedural variants.
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Zhang, Paige, Kathryn Wiens, Ri Wang, Linh Luong, Donna Ansara, Stephanie Gower, Kate Bassil, and Stephen W. Hwang. "Cold Weather Conditions and Risk of Hypothermia Among People Experiencing Homelessness: Implications for Prevention Strategies." International Journal of Environmental Research and Public Health 16, no. 18 (September 5, 2019): 3259. http://dx.doi.org/10.3390/ijerph16183259.
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Hypothermia is a preventable condition that disproportionately affects individuals who experience homelessness, yet limited data exist to inform the response to cold weather. To fill this gap, we examined the association between meteorological conditions and the risk of hypothermia among homeless individuals. Hypothermic events were identified from emergency department charts and coroner’s records between 2004 and 2015 in Toronto, Canada. A time-stratified case-crossover design with conditional logistic regression was used to assess the relationship between the meteorological conditions (minimum temperature and precipitation) and the risk of hypothermia. There were 97 hypothermic events identified: 79 injuries and 18 deaths. The odds of experiencing a hypothermic event increased 1.64-fold (95% CI: 1.30–2.07) with every 5 °C decrease in the minimum daily temperature and 1.10-fold (95% CI: 1.03–1.17) with every 1 mm increase in precipitation. The risk of hypothermia among individuals experiencing homelessness increased with declining temperature; however, most cases occurred during periods of low and moderate cold stress. 72% occurred when the minimum daily temperatures were warmer than −15 °C. These findings highlight the importance of providing a seasonal cold weather response to prevent hypothermia, complemented by an alert-based response on extremely cold days.
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Carr, Jennie M., and Steven L. Lima. "Nocturnal hypothermia impairs flight ability in birds: a cost of being cool." Proceedings of the Royal Society B: Biological Sciences 280, no. 1772 (December 7, 2013): 20131846. http://dx.doi.org/10.1098/rspb.2013.1846.
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Many birds use regulated drops in night-time body temperature ( T b ) to conserve energy critical to winter survival. However, a significant degree of hypothermia may limit a bird's ability to respond to predatory attack. Despite this likely energy–predation trade-off, the behavioural costs of avian hypothermia have yet to be examined. We thus monitored the nocturnal hypothermia of mourning doves ( Zenaida macroura ) in a laboratory setting in response to food deprivation. Nocturnal flight tests were used to quantify the flight ability of hypothermic doves. Many hypothermic doves (39% of tests) could not fly while carrying a small weight, but could do so after quickly warming up to typical daytime T b . Doves that were unable to fly during their first test were more hypothermic than those that could fly, with average T b reductions of 5.3°C and 3.3°C, respectively, but there was no overall indication of a threshold T b reduction beyond which doves were consistently incapable of flight. These results suggest that energy-saving hypothermia interferes with avian antipredator behaviour via a reduction in flight ability, likely leading to a trade-off between energy-saving hypothermia and the risk of predation.
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Watters, Marianne, Hilary Wilson, and Pamela Everitt. "Phenytoin-induced hypothermia." BMJ Case Reports 12, no. 1 (January 2019): e227443. http://dx.doi.org/10.1136/bcr-2018-227443.
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A 60-year-old man with cerebral palsy and epilepsy was admitted with acute lethargy and deterioration in coordination. He was noted to be hypothermic at 35°C on admission. Routine work-up revealed toxic levels of phenytoin. No cause of hypothermia could be identified but as his phenytoin levels normalised, his body temperature also improved. There are three other reported cases of phenytoin- induced hypothermia in the literature. Could this be a rare cause of hypothermia?
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Li, Tao, Xiulai Lin, Yu Zhu, Lijie Li, and Liangming Liu. "Short-term, Mild Hypothermia Can Increase the Beneficial Effect of Permissive Hypotension on Uncontrolled Hemorrhagic Shock in Rats." Anesthesiology 116, no. 6 (June 1, 2012): 1288–98. http://dx.doi.org/10.1097/aln.0b013e318256f09d.
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Background Our previous and other studies have shown that hypotensive or hypothermic resuscitation have beneficial effects on uncontrolled hemorrhagic shock. Whether hypothermia can increase the beneficial effect of hypotensive resuscitation on hemorrhagic shock is not known. Methods Two-hundred and twenty Sprague-Dawley rats were used to make uncontrolled hemorrhagic shock. Before bleeding was controlled, rats received normotensive or hypotensive resuscitation (target mean arterial pressure at 80 or 50 mmHg) in combination with normal (37°C) or mild hypothermia (34°C) (phase II). After bleeding was controlled, rats received whole blood and lactated Ringer's solution resuscitation for 2 h (phase III). The animal survival, blood loss, fluid requirement, cardiac output, and coagulation functions, as well as vital organ function, mitochondrial function, and energy metabolism of liver, kidney and intestines, were noted. Results Short-term, mild hypothermia before bleeding was controlled increased the beneficial effect of hypotensive resuscitation. Hypothermia further decreased blood loss, oxygen consumption, and functional damage to the liver, kidney, and intestines during hypotensive resuscitation, protected mitochondrial function and energy metabolism (activity of Na(+)-K(+)-ATPase), and further improved survival time and survival rate (hypothermic/hypotensive combined group: survival rate, 9/10; survival time, 616 min; normothermic/normotensive group: 1/10, 256 min; hypothermic/normotensive group: 4/10, 293 min). Hypothermia slightly inhibited coagulation function. Conclusion Mild hypothermia before bleeding is controlled can increase the beneficial effect of hypotensive resuscitation on uncontrolled hemorrhagic shock. The mechanism underlying the benefits of short-term hypothermia may be related to the decrease in oxygen consumption and metabolism, and protection of mitochondrial and organ functions.
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Westermaier, Thomas, Stefan Zausinger, Alexander Baethmann, Hans-Jakob Steiger, and Robert Schmid-Elsaesser. "No additional neuroprotection provided by barbiturate-induced burst suppression under mild hypothermic conditions in rats subjected to reversible focal ischemia." Journal of Neurosurgery 93, no. 5 (November 2000): 835–44. http://dx.doi.org/10.3171/jns.2000.93.5.0835.
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Object. Mild-to-moderate hypothermia is increasingly used for neuroprotection in humans. However, it is unknown whether administration of barbiturate medications in burst-suppressive doses—the gold standard of neuroprotection during neurovascular procedures—provides an additional protective effect under hypothermic conditions. The authors conducted the present study to answer this question.Methods. Thirty-two Sprague—Dawley rats were subjected to 90 minutes of middle cerebral artery occlusion and randomly assigned to one of four treatment groups: 1) normothermic controls; 2) methohexital treatment (burst suppression); 3) induction of mild hypothermia (33°C); and 4) induction of mild hypothermia plus methohexital treatment (burst suppression). Local cerebral blood flow was continuously monitored using bilateral laser Doppler flowmetry and electroencephalography. Functional deficits were quantified and recorded during daily neurological examinations. Infarct volumes were assessed histologically after 7 days. Methohexital treatment, mild hypothermia, and mild hypothermia plus methohexital treatment reduced infarct volumes by 32%, 71%, and 66%, respectively, compared with normothermic controls. Furthermore, mild hypothermia therapy provided the best functional outcome, which was not improved by additional barbiturate therapy.Conclusions. The results of this study indicate that barbiturate-induced burst suppression is not required to achieve maximum neuroprotection under mild hypothermic conditions. The magnitude of protection afforded by barbiturates alone appears to be modest compared with that provided by mild hypothermia.
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Kawai, Kensuke, Hitoshi Nakayama, and Akira Tamura. "Limited but Significant Protective Effect of Hypothermia on Ultra-Early-Type Ischemic Neuronal Injury in the Thalamus." Journal of Cerebral Blood Flow & Metabolism 17, no. 5 (May 1997): 543–52. http://dx.doi.org/10.1097/00004647-199705000-00008.
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We investigated the protective effect of hypothermia on ultra-early-type ischemic injury in the thalamic reticular nucleus of the rat. Cerebral ischemia was produced by 5 min of cardiac arrest followed by resuscitation. Rectal and cranial temperature during and after cardiac arrest was maintained at 37–38°C in the normothermic group and at 32–33°C in the hypothermic group. In the postischemic hypothermic group, temperature was maintained at 32–33°C starting 15 min after normothermic ischemia. Histological damage was evaluated quantitatively. While after 5 min of recirculation there was no difference in morphological changes in terms of neuronal halo formation, intraischemic hypothermia reduced the severity of the degenerative changes represented by vacuolated or dark neurons by 15 min. Postischemic hypothermia failed to show any evidence of protection by 30 min. The protective effect of intraischemic hypothermia remained significant when evaluated at 14 days after ischemia by volumetry of the lesion and neuronal density analysis, whereas postischemic hypothermia had no clear protective effect. These results suggest that the protective effect of intraischemic hypothermia applies to neurons susceptible to ultra-early-type injury, but the effect of postischemic hypothermia is limited because normothermic ischemia results in extensive degeneration in these neurons by 15 min.
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Dietrich, W. Dalton, Raul Busto, Ofelia Alonso, Mordecai Y. T. Globus, and Myron D. Ginsberg. "Intraischemic but Not Postischemic Brain Hypothermia Protects Chronically following Global Forebrain Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (July 1993): 541–49. http://dx.doi.org/10.1038/jcbfm.1993.71.
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We investigated whether postischemic brain hypothermia (30°C) would permanently protect the hippocampus following global forebrain ischemia. Global ischemia was produced in anesthetized rats by bilateral carotid artery occlusion plus hypotension (50 mm Hg). In the postischemic hypothermic group, brain temperature was maintained at 37°C during the 10-min ischemic insult but reduced to 30°C starting 3 min into the recirculation period and maintained at 30°C for 3 h. In normothermic animals, intra- and postischemic brain temperature was maintained at 37°C. After recovery for 3 days, 7 days, or 2 months, the extent of CA1 hippocampal histologic injury was quantitated. At 3 days after ischemia, postischemic hypothermia significantly protected the hippocampal CA1 sector compared with normothermic animals. For example, within the medial, middle, and lateral CA1 subsectors, the numbers of normal neurons were increased 20-, 13-, and 9-fold by postischemic hypothermia (p < 0.01). At 7 days after the ischemic insult, however, the degree of postischemic hypothermic protection was significantly reduced. In this case, the numbers of normal neurons were increased an average of only threefold compared with normothermia. Ultrastructural analysis of 7-day postischemic hypothermic rats demonstrated CA1 pyramidal neurons showing variable degrees of injury surrounded by reactive astrocytes and microglial cells. At 2 months after the ischemic insult, no trend for protection was demonstrated. In contrast to postischemic hypothermia, significant protection was seen at 2 months following intraischemic hypothermia. These data indicate that intraischemic, but not postischemic, brain hypothermia provides chronic protection to the hippocampus after transient brain ischemia. The inability of postischemic hypothermia to protect chronically after 3 days could indicate that (a) postischemic hypothermia merely delays ischemic cell death and/or (b) the postischemic brain undergoes a secondary insult. In postischemic treatment protocols, chronic survival studies are required to determine accurately the ultimate histopathological outcome following global cerebral ischemia.
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Troutman, Gregory Scott, Jason Salamon, Matthew Scharf, and Jeremy A. Mazurek. "Cold at the Core: Osborn Waves in Neurosarcoidosis-Induced Central Hypothermia." Case Reports in Cardiology 2019 (January 15, 2019): 1–3. http://dx.doi.org/10.1155/2019/5845839.
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Osborn waves, or J waves, initially described by John Osborn in 1953 in hypothermic dog experiments, are highly sensitive and specific for hypothermia. Initially thought to be secondary to a hypothermia-induced “injury current,” they have more recently been attributed to a voltage differential between epicardial and endocardial potassium (Ito) currents. While the exact conditions required to induce such waves have been debated, numerous clinical scenarios of environmental and iatrogenic hypothermia have been described. Below, we report a novel case of hypothermia—that of neurosarcoidosis-induced central hypothermia with resultant Osborn waves and other associated findings found on electrocardiogram (ECG).
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Gutierrez, G., A. R. Warley, and D. R. Dantzker. "Oxygen delivery and utilization in hypothermic dogs." Journal of Applied Physiology 60, no. 3 (March 1, 1986): 751–57. http://dx.doi.org/10.1152/jappl.1986.60.3.751.
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Hypothermia produces a decrease in metabolic rate that may be beneficial under conditions of reduced O2 delivery (Do2). Another effect of hypothermia is to increase the affinity of hemoglobin for O2, which can adversely affect the release of O2 to the tissues. To determine the overall effect of hypothermia on the ability of the peripheral tissues to extract O2 from blood, we compared the response to hypoxemia of hypothermic dogs (n = 8) and of normothermic controls (n = 8). The animals were anesthetized, mechanically ventilated, and paralyzed to prevent shivering. The inspired concentration of O2 was progressively reduced until the dogs died. The core temperatures of the control and hypothermic dogs were 37.7 +/- 0.3 and 30.5 +/- 0.1 degree C, respectively (P less than 0.01). The O2 consumption (VO2) of the control dogs was significantly greater than that of the hypothermic dogs (P less than 0.05), being 4.7 +/- 0.4 and 3.2 +/- 0.3 ml X min-1 X kg-1, respectively. Hypothermia produced a left shift of the oxyhemoglobin dissociation curve (ODC) to a PO2 at which hemoglobin is half-saturated with O2 of 19.8 +/- 0.7 Torr (control = 32.4 +/- 0.7 Torr, P less than 0.01). The O2 delivery at which the VO2 becomes supply dependent (DO2crit) was 8.5 ml X min-1 X kg-1 for control and 6.2 ml X min-1 X kg-1 for hypothermia. The hypothermic dogs maintained their base-line VO2′s at lower arterial PO2′s than control.(ABSTRACT TRUNCATED AT 250 WORDS)
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O’Brien, Caitlin E., Polan T. Santos, Ewa Kulikowicz, Michael Reyes, Raymond C. Koehler, Lee J. Martin, and Jennifer K. Lee. "Hypoxia-Ischemia and Hypothermia Independently and Interactively Affect Neuronal Pathology in Neonatal Piglets with Short-Term Recovery." Developmental Neuroscience 41, no. 1-2 (2019): 17–33. http://dx.doi.org/10.1159/000496602.
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Therapeutic hypothermia is the standard of clinical care for moderate neonatal hypoxic-ischemic encephalopathy. We investigated the independent and interactive effects of hypoxia-ischemia (HI) and temperature on neuronal survival and injury in basal ganglia and cerebral cortex in neonatal piglets. Male piglets were randomized to receive HI injury or sham procedure followed by 29 h of normothermia, sustained hypothermia induced at 2 h, or hypothermia with rewarming during fentanyl-nitrous oxide anesthesia. Viable and injured neurons and apoptotic profiles were counted in the anterior putamen, posterior putamen, and motor cortex at 29 h after HI injury or sham procedure. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) identified genomic DNA fragmentation to confirm cell death. Though hypothermia after HI preserved viable neurons in the anterior and posterior putamen, hypothermia prevented neuronal injury in only the anterior putamen. Hypothermia initiated 2 h after injury did not protect against apoptotic cell death in either the putamen or motor cortex, and rewarming from hypothermia was associated with increased apoptosis in the motor cortex. In non-HI shams, sustained hypothermia during anesthesia was associated with neuronal injury and corresponding viable neuron loss in the anterior putamen and motor cortex. TUNEL confirmed increased neurodegeneration in the putamen of hypothermic shams. Anesthetized, normothermic shams did not show abnormal neuronal cytopathology in the putamen or motor cortex, thereby demonstrating minimal contribution of the anesthetic regimen to neuronal injury during normothermia. We conclude that the efficacy of hypothermic protection after HI is region specific and that hypothermia during anesthesia in the absence of HI may be associated with neuronal injury in the developing brain. Studies examining the potential interactions between hypothermia and anesthesia, as well as with longer durations of hypothermia, are needed.
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Savioli, Gabriele, Iride Francesca Ceresa, Gaia Bavestrello Piccini, Nicole Gri, Alba Nardone, Raffaele La Russa, Angela Saviano, Andrea Piccioni, Giovanni Ricevuti, and Ciro Esposito. "Hypothermia: Beyond the Narrative Review—The Point of View of Emergency Physicians and Medico-Legal Considerations." Journal of Personalized Medicine 13, no. 12 (December 5, 2023): 1690. http://dx.doi.org/10.3390/jpm13121690.
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Hypothermia is a widespread condition all over the world, with a high risk of mortality in pre-hospital and in-hospital settings when it is not promptly and adequately treated. In this review, we aim to describe the main specificities of the diagnosis and treatment of hypothermia through consideration of the physiological changes that occur in hypothermic patients. Hypothermia can occur due to unfavorable environmental conditions as well as internal causes, such as pathological states that result in reduced heat production, increased heat loss or ineffectiveness of the thermal regulation system. The consequences of hypothermia affect several systems in the body—the cardiovascular system, the central and peripheral nervous systems, the respiratory system, the endocrine system and the gastrointestinal system—but also kidney function, electrolyte balance and coagulation. Once hypothermia is recognized, prompt treatment, focused on restoring body temperature and supporting vital functions, is fundamental in order to avert preventable death. It is important to also denote the fact that CPR has specificities related to the unique profile of hypothermic patients.
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Wang, Bing, Jillian S. Armstrong, Jeong-Hoo Lee, Utpal Bhalala, Ewa Kulikowicz, Hui Zhang, Michael Reyes, et al. "Rewarming from Therapeutic Hypothermia Induces Cortical Neuron Apoptosis in a Swine Model of Neonatal Hypoxic–Ischemic Encephalopathy." Journal of Cerebral Blood Flow & Metabolism 35, no. 5 (January 7, 2015): 781–93. http://dx.doi.org/10.1038/jcbfm.2014.245.
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The consequences of therapeutic hypothermia for neonatal hypoxic–ischemic encephalopathy are poorly understood. Adverse effects from suboptimal rewarming could diminish neuroprotection from hypothermia. Therefore, we tested whether rewarming is associated with apoptosis. Piglets underwent hypoxia–asphyxia followed by normothermic or hypothermic recovery at 2 hours. Hypothermic groups were divided into those with no rewarming, rewarming at 0.5 °C/hour, or rewarming at 4 °C/hour. Neurodegeneration at 29 hours was assessed by hematoxylin and eosin staining, TUNEL assay, and immunoblotting for cleaved caspase-3. Rewarmed piglets had more apoptosis in motor cortex than did those that remained hypothermic after hypoxia–asphyxia. Apoptosis in piriform cortex was greater in hypoxic–asphyxic, rewarmed piglets than in naive/sham piglets. Caspase-3 inhibitor suppressed apoptosis with rewarming. Rapidly rewarmed piglets had more caspase-3 cleavage in cerebral cortex than did piglets that remained hypothermic or piglets that were rewarmed slowly. We conclude that rewarming from therapeutic hypothermia can adversely affect the newborn brain by inducing apoptosis through caspase mechanisms.
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Kato, Atsushi, Saurabh Singh, Kenneth R. McLeish, Michael J. Edwards, and Alex B. Lentsch. "Mechanisms of hypothermic protection against ischemic liver injury in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 4 (April 1, 2002): G608—G616. http://dx.doi.org/10.1152/ajpgi.00454.2001.
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Hepatic hypothermia can safely prolong the duration of hepatic inflow occlusion during complex liver resectional surgeries. The mechanism(s) by which hypothermia protects against this form of liver ischemia-reperfusion injury are not completely understood. In this study, we sought to determine whether hypothermia protects against ischemia-reperfusion injury by altering the hepatic inflammatory response. Mice undergoing 90 min of partial hepatic ischemia followed by up to 8 h of reperfusion had their body temperatures regulated at 35–37°C (normothermic) or unregulated, in which rectal temperature dropped as low as 25°C by the end of ischemia (hypothermic). Hypothermic mice had less liver injury vs. normothermic mice, as assessed histologically, by serum transaminase levels (89% decrease), and by liver wet-to-dry weight ratios (91% decrease). Neutrophil accumulation was absent in hypothermic mice (99% reduction vs. normothermic mice). Production of the proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and macrophage inflammatory protein-2 were reduced by up to 92%. Activation of the transcription factor nuclear factor-κB was not reduced in hypothermic mice, but activation of c-Jun NH2-terminal kinase (JNK) and the transcription factor activator protein (AP)-1 were greatly diminished. These data suggest that hypothermia suppresses the hepatic inflammatory response through selective inhibition of JNK and AP-1.
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Frietsch, Thomas, Peter Krafft, Axel Piepgras, Christian Lenz, Wolfgang Kuschinsky, and Klaus F. Waschke. "Relationship between Local Cerebral Blood Flow and Metabolism during Mild and Moderate Hypothermia in Rats." Anesthesiology 92, no. 3 (March 1, 2000): 754–63. http://dx.doi.org/10.1097/00000542-200003000-00019.
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Background Hypothermia may interfere with the relationship between cerebral blood flow (CBF) and metabolism. Because this conclusion was based on the analysis of global values, the question remains whether hypothermic CBF/metabolism uncoupling exists on a local cerebral level. This study investigated the effects of hypothermic anesthesia on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU). Methods Thirty-six rats were anesthetized with isoflurane (1 minimum alveolar concentration) and artificially ventilated to maintain normal arterial carbon dioxide partial pressure (pH-stat). Pericranial temperature was maintained as normothermic (37.5 degrees C, n = 12) or was reduced to 35 degrees C (n = 12) or 32 degrees C (n = 12). Pericranial temperature was maintained constant for 60 min until LCBF or LCGU were measured by autoradiography. Twelve conscious rats served as normothermic controls. Results Compared with conscious animals, mean CBF remained unchanged during normothermic anesthesia. Mean CBF significantly increased during mild hypothermia but was unchanged during moderate hypothermia. During normothermic anesthesia, mean CGU was 45% lower than in conscious controls (P < 0.05). No further CGU reduction was found during mild hypothermia, whereas CGU further decreased during moderate hypothermia (48%; P < 0.05). Local analysis showed a linear LCBF/LCGU relationship in conscious (r = 0.94) and anesthetized (r = 0.94) normothermic animals, as well as in both hypothermic groups (35 degrees C: r = 0.92; 32 degrees C: r = 0.95; P < 0.05). The LCBF-to-LCGU ratio increased from 1.4 (conscious controls) to 2.4 (normothermic isoflurane) and 3.6 ml/micromol (mild and moderate hypothermia, P < 0.05). Conclusions Decrease of mean CGU at unchanged or increased mean CBF during hypothermic anesthesia may not indicate uncoupling. Local analysis shows a maintained linear relationship that is reset to a higher CBF/CGU ratio.
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Hoo-Paris, R., M. L. Jourdan, L. C. Wang, and R. Rajotte. "Insulin secretion and substrate homeostasis in prolonged hypothermia in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 6 (December 1, 1988): R1035—R1040. http://dx.doi.org/10.1152/ajpregu.1988.255.6.r1035.
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In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.
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Hackenhaar, Fernanda S., Tássia M. Medeiros, Fernanda M. Heemann, Camile S. Behling, Jordana S. Putti, Camila D. Mahl, Cleber Verona, et al. "Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/8704352.
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After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.
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Akarsu, Eyup S., and Soner Mamuk. "Escherichia coli lipopolysaccharides produce serotype-specific hypothermic response in biotelemetered rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 5 (May 2007): R1846—R1850. http://dx.doi.org/10.1152/ajpregu.00786.2006.
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We investigated whether LPS-induced hypothermia develops in a serotype-specific manner in biotelemetered conscious rats. Two different Escherichia coli serotypes of LPSs were injected at a dose of 250 μg/kg ip. E. coli O55:B5 LPS elicited an initial hypothermia and subsequent fever, but E. coli O111:B4 LPS caused more potent monophasic hypothermia. Serum tumor necrosis factor (TNF)-α levels were dramatically elevated at the initial phase of the hypothermia induced by both LPSs. This elevation tended to subside at the nadir of E. coli O55:B5 LPS-induced response but progressively increased at the nadir of E. coli O111:B4 LPS hypothermia. Serum IL-10 levels were moderately elevated at the initial phase of the hypothermia and persisted at the same level at the nadir of each LPS-induced response. No change was observed at the serum IL-18 levels. A selective cyclooxygenase (COX)-1 enzyme inhibitor, valeryl salicylate (20 mg/kg sc), abolished the hypothermia without any effect on the elevated cytokine levels. Another COX-1-selective inhibitor, 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC-560; 1 mg/kg sc) inhibited hypothermic responses as well. Meanwhile, cytokine levels were also reduced by SC-560 treatment. These findings suggest that LPS-induced hypothermia may have serotype-specific characteristics in rats. E. coli O111:B4 LPS has more potent hypothermic activity than E. coli O55:B5 LPS; that may presumably be related to its higher or sustained capability to release antipyretic cytokines, such as TNF-α. COX-1 enzyme may be involved in the generation of the hypothermia, regardless of the type of LPS administered.
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Kozlov, B. N., D. S. Panfilov, E. L. Sonduev, and I. V. Ponomarenko. "Early postoperative effects of the hypothermia level during hypothermic circulatory arrest in patients with ascending aortic aneurysm." Russian Journal of Cardiology 25, no. 8 (September 14, 2020): 3419. http://dx.doi.org/10.15829/1560-4071-2020-3419.
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Aim. To compare the effectiveness and safety of ascending aortic hemiarch replacement performed during hypothermic circulatory arrest with different temperature regimens.Material and methods. The study included 104 patients with ascending aortic aneurysm, who underwent ascending aortic hemiarch replacement under hypothermic circulatory arrest and antegrade cerebral perfusion. Depending on the temperature regimen, all patients were divided into two comparable groups: group 1 (n=28) — patients operated on under mild hypothermia (29-31oС), group 2 (n=76) — patients operated on under moderate hypothermia (25-28oC).Results. Comparative analysis of intraoperative data between groups of patients with mild and moderate hypothermia revealed a significant difference in the duration of cardiopulmonary bypass (111 [97; 135] min vs 125 [108.5; 170] min, p=0,031) and surgery (240 [210; 270 ] min vs 275 [240; 330] min, p=0,003). In the early postoperative period, the best results were also obtained in patients of mild hypothermia group. In these patients, compared with moderate hypothermia group, there was a lower frequency of reoperation due to bleeding (3,5% vs 5,2%, p=0,572), a decrease in transfused fresh frozen plasma volume (2 [2; 4] vs 4 [2; 4], p=0,03), a decrease in the ventilatory support duration (10 [7; 16] hours vs 18 [10; 24] hours, p=0,002), as well as a bed-day decrease in intensive care unit (2 [2; 3] and 3 [2; 4] days, p=0,005). No neurologic deficit was found in any of the patients. In-hospital mortality had no significant intergroup differences (p=0,541).Conclusion. An increase in the temperature regimen during the ascending aortic hemiarch replacement performed under hypothermic circulatory arrest is relatively safe in relation to early postoperative complications. Mild hypothermia does not increase early postoperative surgical risks compared to moderate hypothermia.
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Kim, Soo Hyun, Ji Hye Hwang, Jiyoon Jeong, Jeong Min Lee, Ha Na Lee, Sung Hyeon Park, Byong Sop Lee, and Euiseok Jung. "Association of Moderate Hypothermia at Admission with Short-Term and Long-Term Outcomes in Extremely Low Birth Weight Infants." Neonatal Medicine 30, no. 2 (May 31, 2023): 28–33. http://dx.doi.org/10.5385/nm.2023.30.2.28.
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Purpose: Extremely low birth weight (ELBW) infants exhibit immature thermoregulation and are easily exposed to hypothermia. We investigated the association between hypothermia on admission with short- and long-term outcomes.Methods: Medical records of ELBW infants admitted to the neonatal intensive care unit of a tertiary medical center between June 2012 and February 2017 were retrospectively analyzed. Upon admission, the axillary body temperature was measured. Moderate hypothermia was defined as admission temperature below 36 ℃.Results: A total of 208 infants with gestational age of 26.4±2.3 weeks and birth weight of 746.7±154.9 g were included. Admission temperature ranged from 33.5 to 36.8 ℃ (median 36.1 ℃). Univariate analyses of maternal and infant characteristics were performed for moderately hypothermic and control (normothermic to mildly hypothermic) infants. Lower gestational age, lower birth weight, and vaginal delivery correlated with moderate hypothermia. Logistic regression analyses adjusted for confounders revealed that the incidence of hemodynamically significant patent ductus arteriosus (hsPDA) was associated with moderate hypothermia in ELBW infants. Moreover, abnormal mental developmental index scores on the Bayley Scales of Infant Development II at a corrected age of 18 to 24 months were associated with moderate hypothermia, but not with the psychomotor developmental index, incidence of blindness, deafness, or cerebral palsy.Conclusion: Moderate hypothermia at admission is not only correlated with short-term neonatal morbidities such as hsPDA, but may also be associated with long-term neurodevelopmental impairment in ELBW infants. Future large-scale studies are required to clarify the long-term consequences of hypothermia upon admission.
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Weuster, Matthias, Philipp Mommsen, Roman Pfeifer, Juliane Mohr, Steffen Ruchholtz, Sascha Flohé, Matthias Fröhlich, et al. "Induced Hypothermia Does Not Harm Hemodynamics after Polytrauma: A Porcine Model." Mediators of Inflammation 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/829195.
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Background. The deterioration of hemodynamics instantly endangers the patients’ life after polytrauma. As accidental hypothermia frequently occurs in polytrauma, therapeutic hypothermia still displays an ambivalent role as the impact on the cardiopulmonary function is not yet fully understood.Methods. We have previously established a porcine polytrauma model including blunt chest trauma, penetrating abdominal trauma, and hemorrhagic shock. Therapeutic hypothermia (34°C) was induced for 3 hours. We documented cardiovascular parameters and basic respiratory parameters. Pigs were euthanized after 15.5 hours.Results. Our polytrauma porcine model displayed sufficient trauma impact. Resuscitation showed adequate restoration of hemodynamics. Induced hypothermia had neither harmful nor major positive effects on the animals’ hemodynamics. Though heart rate significantly decreased and mixed venous oxygen saturation significantly increased during therapeutic hypothermia. Mean arterial blood pressure, central venous pressure, pulmonary arterial pressure, and wedge pressure showed no significant differences comparing normothermic trauma and hypothermic trauma pigs during hypothermia.Conclusions. Induced hypothermia after polytrauma is feasible. No major harmful effects on hemodynamics were observed. Therapeutic hypothermia revealed hints for tissue protective impact. But the chosen length for therapeutic hypothermia was too short. Nevertheless, therapeutic hypothermia might be a useful tool for intensive care after polytrauma. Future studies should extend therapeutic hypothermia.
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Mustonen, Caius, Hannu-Pekka Honkanen, Siri Lehtonen, Hannu Tuominen, Tuomas Mäkelä, Timo Kaakinen, Kai Kiviluoma, Vesa Anttila, and Tatu Juvonen. "Moderate hypothermia with remote ischaemic preconditioning improves cerebral protection compared to deep hypothermia: a study using a surviving porcine model." European Journal of Cardio-Thoracic Surgery 58, no. 2 (April 1, 2020): 269–76. http://dx.doi.org/10.1093/ejcts/ezaa065.
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Abstract OBJECTIVES The optimal temperature management of hypothermic circulatory arrest is still controversial. Moderate hypothermia preserves cerebral autoregulation and shortens cardiopulmonary bypass (CPB) duration. However, moderate hypothermia alone has inferior organ protection to deep hypothermia, so adjuncts that increase the ischaemic tolerance are needed. Thus, we hypothesized that a combination of remote ischaemic preconditioning (RIPC) and moderate hypothermia would be superior to deep hypothermia alone. METHODS Sixteen pigs were randomized to either RIPC or control groups (8 + 8). The RIPC group underwent 4 cycles of transient hind limb ischaemia. The RIPC group underwent cooling with CPB to 24°C, and the control group underwent cooling with CPB to 18°C, followed by a 30-min arrest period and subsequent rewarming to 36°C. Measurements of cerebral metabolism were made from sagittal sinus blood samples and common carotid artery blood flow. The permissible periods of hypothermic circulatory arrest were calculated based on these measurements. Neurological recovery was evaluated daily during a 7-day follow-up, and the brain was harvested for histopathological analysis. RESULTS Six pigs in the RIPC group reached normal neurological function, but none in the control group reached normal neurological function (P = 0.007). The composite neurological score of all postoperative days was higher in the RIPC group than in the control group [55 (52–58) vs 45 (39–51), P = 0.026]. At 24°C, the estimated permissible periods of hypothermic circulatory arrest were 21 (17–25) min in the RIPC group and 11 (9–13) min in the control group (P = 0.007). CONCLUSIONS RIPC combined with moderate hypothermia provides superior cerebral protection.
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Otworowski, Maciej, Krzysztof Sośnicki, Elżbieta Cipora, and Andrzej Kotela. "Prehospital management of accidental hypothermia." Emergency Medical Service 7, no. 4 (2020): 306–12. http://dx.doi.org/10.36740/emems202004110.
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The accidental hypothermia can be diagnosed if a body temperature fall below the 35°C. It is frequently encountered in Poland. It was the cause of death of 1836 people between 2009 and 2012. The aim of our paper was to present the current state of the art regarding prehospital management of the hypothermic patient. The gold standard of internal body temperature measurement is by an esophageal probe. The hypothermic patient should be handled very carefully. The wet clothes should be cut and the patient should be covered with insulation materials. Active rewarming should be initiated in all of the patients in severe and mild hypothermia. After finding an unconscious person who is likely to be in hypothermia, the search for signs of life should take 60 seconds. When CPR is started it should be conducted with standard protocols. Infusion fluids should be heated and the preferred ones are: 0,9% NaCl and crystalloids. No antiarrhythmic or vasoconstrictive drugs should be given in patients with internal body temperature below 30°C. Conclusions: We should encourage providers to equip the rescue teams with the active rewarming devices and insulation materials. The prevention of further heat loss in hypothermic patient is of the greatest importance. The life support should be centered around cardiopulmonary resuscitation with quality chest compressions and adequate ventilation. The definitive treatment of patients suffering from deep hypothermia is most effective in specialist centres dedicated to treating this condition. Air transportation is preferred to land transportation.
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Frappell, P., K. Westwood, and M. Maskrey. "Ventilatory and metabolic responses to hypoxia during moderate hypothermia in anesthetized rats." Journal of Applied Physiology 79, no. 1 (July 1, 1995): 256–60. http://dx.doi.org/10.1152/jappl.1995.79.1.256.
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In resting euthermic mammals, hypoxia elicits a hyperventilation that results from a combination of hyperpnea and hypometabolism. Often accompanying the hypoxia-induced hypometabolism is a drop in body temperature. To separate the synergic effects of hypothermia per se from the direct effects of hypoxia on metabolic rate, ventilation (VE), and O2 consumption (VO2) were measured in anesthetized rats fitted with abdominal heat exchangers and maintained at either normothermic (37.5 degrees C) or hypothermic (35 degrees C) body temperatures while exposed to either normoxia or hypoxia (7% O2). Hypothermia induced parallel decreases in VE and VO2, thereby maintaining VE/VO2. Hypoxia resulted in a hyperventilation achieved with the same relative decrease in VO2 and increase in VE in both normothermic and hypothermic rats. The results suggest that 1) the changes in metabolic rate and VE during hypothermia reflect a direct effect of cold and, 2) because of similar levels of hypoxic hyperventilation in the hypothermic and normothermic rats, relative to metabolic rate, respiratory gain has not been depressed in hypothermic rats.
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Roeker, Lindsey E., Vinay Gupta, Wilson I. Gonsalves, Alexandra P. Wolanskyj, and Naseema Gangat. "Cyclic Bicytopenia in a Patient with Shapiro Syndrome." Case Reports in Hematology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/231713.
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Shapiro syndrome and periodic hypothermia have been reported approximately fifty times in the literature. Shapiro syndrome is defined as the constellation of periodic hypothermia and hyperhidrosis along with agenesis of the corpus callosum by Shapiro et al. in 1969. Periodic hypothermia is a more broad diagnosis with a number of proposed mechanisms; it occurs in patients without structural brain abnormalities. Hematologic abnormalities beyond iron-deficiency anemia have not been documented in any of the reported cases of Shapiro syndrome or periodic hypothermia. Though accidental and therapeutic hypothermia have been associated with thrombocytopenia, this is, to our knowledge, the first reported case of periodic intrinsic hypothermia causing bicytopenia. In this report, we present the case of a patient with Shapiro syndrome who experienced cyclic bicytopenia mirroring hypothermic episodes. We address the differential diagnosis of bicytopenia, review the mechanisms proposed for cytopenias related to hypothermia, and propose possible mechanisms for the finding in this case.
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Ning, Xue-Han, Shi-Han Chen, Cheng-Su Xu, Linheng Li, Lena Y. Yao, Kun Qian, Julia J. Krueger, Outi M. Hyyti, and Michael A. Portman. "Selected Contribution: Hypothermic protection of the ischemic heart via alterations in apoptotic pathways as assessed by gene array analysis." Journal of Applied Physiology 92, no. 5 (May 1, 2002): 2200–2207. http://dx.doi.org/10.1152/japplphysiol.01035.2001.
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Hypothermia improves resistance to ischemia in the cardioplegia-arrested heart. This adaptive process produces changes in specific signaling pathways for mitochondrial proteins and heat-shock response. To further test for hypothermic modulation of other signaling pathways such as apoptosis, we used various molecular techniques, including cDNA arrays. Isolated rabbit hearts were perfused and exposed to ischemic cardioplegic arrest for 2 h at 34°C [ischemic group (I); n = 13] or at 30°C before and during ischemia [hypothermic group (H); n = 12]. Developed pressure, the maximum first derivative of left ventricular pressure, oxygen consumption, and pressure-rate product ( P < 0.05) recovery were superior in H compared with in I during reperfusion. mRNA expression for the mitochondrial proteins, adenine translocase and the β-subunit of F1-ATPase, was preserved by hypothermia. cDNA arrays revealed that ischemia altered expression of 13 genes. Hypothermia modified this response to ischemia for eight genes, six related to apoptosis. A marked, near fivefold increase in transformation-related protein 53 in I was virtually abrogated in H. Hypothermia also increased expression for the anti-apoptotic Bcl-2 homologue Bcl-x relative to I but decreased expression for the proapoptotic Bcl-2 homologue bak. These data imply that hypothermia modifies signaling pathways for apoptosis and suggest possible mechanisms for hypothermia-induced myocardial protection.
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Abdul-Mumin, Alhassan, Naa Adzoa Adzeley Boi-Dsane, Samuel Tomilola Oladokun, Sheila Agyeiwaa Owusu, and Patrick Ansah. "A retrospective data analysis on prevalence and risk factors for hypothermia among sick neonates at presentation to the neonatal intensive care unit of the Tamale Teaching Hospital." PLOS ONE 19, no. 5 (May 16, 2024): e0303159. http://dx.doi.org/10.1371/journal.pone.0303159.
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Neonatal hypothermia, defined as an axillary temperature of <36.5C in a neonate, is common in neonatal intensive care units and is almost universal across all geographic and climatic regions of the world. This is even though environmental temperature is a known risk factor for its occurrence. We conducted a retrospective study in the Neonatal Intensive Care Unit of the Tamale Teaching Hospital (TTH) to document the prevalence and risk factors associated with hypothermia at presentation to the hospital. The study spanned the period from January 2019 to December 2019 and involved all neonates with axillary temperature documented at the time of admission. The prevalence of neonatal hypothermia in this study was 54.76%. Hypothermia was most common in neonates diagnosed with meconium aspiration syndrome (87/105, 82.86%), prematurity and low birth weight (575/702, 81.91%), and birth asphyxia (347/445, 77.98%). Neonates who were delivered vaginally were less likely to develop hypothermia compared to those delivered via Cesarean section. Inborn neonates (delivered in TTH) were 3.2 times more likely to be hypothermic when compared to those who were delivered at home. Neonates with low birth weight and APGAR scores < 7 at 1 and 5 minutes were more likely to be hypothermic. The dry season was found to be protective against hypothermia when compared to the rainy season. The overall mortality rate was 13.68% and the mortality in the subgroup with hypothermia at presentation was 18.87%. Our study documented a high prevalence of hypothermia with higher rates in neonates requiring intervention at birth. It is therefore crucial for perinatal care providers to adhere to the warm chain precautions around the time of birth.
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Hindman, Bradley J. "Cerebral physiology of hypothermia and hypothermic acid-base management during cardiopulmonary bypass." Cardiology in the Young 3, no. 3 (July 1993): 273–80. http://dx.doi.org/10.1017/s1047951100001670.
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Cerebral hypothermia is the principal means of protecting the brain during cardiac surgery, permitting periods of reduced perfusion and/or circulatory arrest. For example, at 10–20°C, circulatory arrest for 45–75 minutes is tolerated in animals without subsequent behavioral or histopathologic evidence of neurologic injury. Nevertheless, clinically, die protective effect of hypothermia is far from complete. In children undergoing hypothermic circulatory arrest under equivalent conditions, coma, seizures, choreoathetosis, and developmental retardation are recognized as potential neurologic sequels, occurring widi a combined incidence of 10-30%. Neurologic complications (stroke, neuropsychologic change) also occur with distressing frequency in adults undergoing cardiac surgery, even in the absence of circulatory arrest. An improved understanding of the physiology of cerebral hypothermia during cardiopulmonary bypass and hypothermic arrest is needed to improve upon these results. This review will address current concepts and controversies regarding flow of blood to the brain and its metabolism during hypothermic cardiopulmonary bypass and their relationship to current techniques for cerebral protection.
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Liu, Elaine, Kevin Lewis, Hiba Al-Saffar, Catherine M. Krall, Anju Singh, Vladimir A. Kulchitsky, Joshua J. Corrigan, et al. "Naturally occurring hypothermia is more advantageous than fever in severe forms of lipopolysaccharide- and Escherichia coli-induced systemic inflammation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 12 (June 15, 2012): R1372—R1383. http://dx.doi.org/10.1152/ajpregu.00023.2012.
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The natural switch from fever to hypothermia observed in the most severe cases of systemic inflammation is a phenomenon that continues to puzzle clinicians and scientists. The present study was the first to evaluate in direct experiments how the development of hypothermia vs. fever during severe forms of systemic inflammation impacts the pathophysiology of this malady and mortality rates in rats. Following administration of bacterial lipopolysaccharide (LPS; 5 or 18 mg/kg) or of a clinical Escherichia coli isolate (5 × 109or 1 × 1010CFU/kg), hypothermia developed in rats exposed to a mildly cool environment, but not in rats exposed to a warm environment; only fever was revealed in the warm environment. Development of hypothermia instead of fever suppressed endotoxemia in E. coli -infected rats, but not in LPS-injected rats. The infiltration of the lungs by neutrophils was similarly suppressed in E. coli -infected rats of the hypothermic group. These potentially beneficial effects came with costs, as hypothermia increased bacterial burden in the liver. Furthermore, the hypotensive responses to LPS or E. coli were exaggerated in rats of the hypothermic group. This exaggeration, however, occurred independently of changes in inflammatory cytokines and prostaglandins. Despite possible costs, development of hypothermia lessened abdominal organ dysfunction and reduced overall mortality rates in both the E. coli and LPS models. By demonstrating that naturally occurring hypothermia is more advantageous than fever in severe forms of aseptic (LPS-induced) or septic ( E. coli -induced) systemic inflammation, this study provides new grounds for the management of this deadly condition.
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Miyazawa, Seiji, Yasutake Shimizu, Takahiko Shiina, Haruko Hirayama, Hironobu Morita, and Tadashi Takewaki. "Central A1-receptor activation associated with onset of torpor protects the heart against low temperature in the Syrian hamster." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 3 (September 2008): R991—R996. http://dx.doi.org/10.1152/ajpregu.00142.2008.
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Body temperature drops dramatically during hibernation, but the heart retains the ability to contract and is resistant to induction of arrhythmia. Although adaptive changes in the heart prior to hibernation may be involved in the cold-resistant property, it remains unclear whether these changes are sufficient for maintaining cardiac pulsatility under an extreme hypothermic condition. We forcibly induced hypothermia in Syrian hamsters by pentobarbital anesthesia combined with cooling of the animals. This allows reproduction of a hypothermic condition in the absence of possible hibernation-specific reactions. Unlike hypothermia in natural hibernation, the forced induction of hypothermia caused atrioventricular block. Furthermore, J-waves, which are typically observed during hypothermia in nonhibernators, were recorded on an ECG. The origin of the J-wave seemed to be related to irreversible injury of the myocardium, because J-waves remained after recovery of body temperature. An abnormal ECG was also found when hypothermia was induced in hamsters that were well adapted to a cold and darkened environment or hamsters that had already experienced hibernation. These results suggest that acclimatization prior to hibernation does not have a crucial effect at least on acquisition of cardiac resistance to low temperature. In contrast, an abnormal ECG was not observed in the case of hypothermia induced by central administration of an adenosine A1-receptor agonist and subsequent cooling, confirming the importance of the adenosine system for inducing hibernation. Our results suggest that some specific mechanisms, which may be driven by a central adenosine system, operate for maintaining the proper cardiac pulsatility under extreme hypothermia.
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Zhu, Junchao, Bing Wang, Jeong-Hoo Lee, Jillian S. Armstrong, Ewa Kulikowicz, Utpal S. Bhalala, Lee J. Martin, Raymond C. Koehler, and Zeng-Jin Yang. "Additive Neuroprotection of a 20-HETE Inhibitor with Delayed Therapeutic Hypothermia after Hypoxia-Ischemia in Neonatal Piglets." Developmental Neuroscience 37, no. 4-5 (2015): 376–89. http://dx.doi.org/10.1159/000369007.
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The severity of perinatal hypoxia-ischemia and the delay in initiating therapeutic hypothermia limit the efficacy of hypothermia. After hypoxia-ischemia in neonatal piglets, the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) has been found to contribute to oxidative stress at 3 h of reoxygenation and to eventual neurodegeneration. We tested whether early administration of a 20-HETE synthesis inhibitor after reoxygenation augments neuroprotection with 3-hour delayed hypothermia. In two hypothermic groups, whole body cooling from 38.5 to 34°C was initiated 3 h after hypoxia-ischemia. Rewarming occurred from 20 to 24 h; then anesthesia was discontinued. One hypothermic group received a 20-HETE inhibitor at 5 min after reoxygenation. A sham-operated group and another hypoxia-ischemia group remained normothermic. At 10 days of recovery, resuscitated piglets with delayed hypothermia alone had significantly greater viable neuronal density in the putamen, caudate nucleus, sensorimotor cortex, CA3 hippocampus, and thalamus than did piglets with normothermic recovery, but the values remained less than those in the sham-operated group. In piglets administered the 20-HETE inhibitor before hypothermia, the density of viable neurons in the putamen, cortex and thalamus was significantly greater than in the group with hypothermia alone. Cytochrome P450 4A, which can synthesize 20-HETE, was expressed in piglet neurons in these regions. We conclude that early treatment with a 20-HETE inhibitor enhances the therapeutic benefit of delayed hypothermia in protecting neurons in brain regions known to be particularly vulnerable to hypoxia-ischemia in term newborns.
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Hayati, Kardina, Syatriawati ., Pitriani ., and Arfah May Syara. "WORKSHOP TREATMENT OF POST SURGICAL HYPOTHERMIC PATIENTS WITH WARMING ELEMENTS ON NURSES IN POST SURGICAL RECOVERY ROOM GRANDMED LUBUK PAKAM HOSPITAL." JURNAL PENGMAS KESTRA (JPK) 2, no. 1 (June 30, 2022): 29–33. http://dx.doi.org/10.35451/jpk.v2i1.1110.
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Surgical procedures have a risk that the integrity or integrity of the body is disturbed and can even cause a life threat to the patient. One of the most at risk was the occurrence of postoperative hypothermia. In the postoperative recovery room, almost all postoperative patients were hypothermic. Nurses in the postoperative room usually provide blankets to warm patients who are hypothermic. This action was less effective to help patients overcome hypothermia. Giving warm fluids was considered effective to help increase the patient's body temperature. This workshop aims to provide knowledge and training on the administration of intravenous fluid heating elements to increase hypothermic body temperature to nurses in the post-surgical recovery room at the Grandmed hospital Lubuk Pakam. The evaluation of this workshop activity was seen from the knowledge of nurses and nurses' skills. Nurses' knowledge and skills were assessed using a questionnaire sheet and pre and post test observations. The results of the workshop showed that as many as 95% of nurses experienced an increase in knowledge and skills in overcoming hypothermia in postoperative patients. This workshop was expected to be able to overcome the problem of hypothermia in postoperative patients and increase the knowledge and skills of nurses.
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Linker, R. A., A. Mohr, L. Cepek, R. Gold, and H. Prange. "Core hypothermia in multiple sclerosis: case report with magnetic resonance imaging localization of a thalamic lesion." Multiple Sclerosis Journal 12, no. 1 (February 2006): 112–15. http://dx.doi.org/10.1191/135248506ms1268cr.
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Hypothermia is a rare condition in multiple sclerosis (MS). We report on a patient with a longstanding secondary progressive MS and six episodes of recurring hypothermia down to 29.98C with associated hypotension, bradycardia, coagulopathy and electrolyte dysequilibrium. Magnetic resonance imaging (MRI) demonstrated severe involvement of the corpus callosum with an associated lesion in the right posterior thalamus. These findings may link hypothermia in MS with callosal and associated thalamic pathology to Shapiro’s syndrome, where agenesis of the corpus callosum and associated abnormalities are related to episodic spontaneous hypothermia. In MS, hypothermic episodes may be triggered by preceding infections, as shown in the present case.