- Scandinavian journal of trauma, resuscitation and emergency medicine
- Published about 3 years ago
The head warming in hypothermic victims is an alternative way of heat donation, which does not inhibit shivering and does not impede the access to the patient’s chest. It seems to be a safe method in mild hypothermia. The authors of the review article “Accidental hypothermia - an update” suggest this way of heat donation, without indicating precisely, in which group of patients it can be applied. In severe hypothermia, the brain-protective effect of cold is well known. The decreased need of oxygen allows good neurological outcome after long lasting cardiac arrest. Therefore, in deep hypothermia, the brain tissue should be rather insulated from the heat source than warmed.
Cold-induced thermogenesis and inflammation-associated cold-seeking behavior are represented by different dorsomedial hypothalamic sites: a three-dimensional functional topography study in conscious rats
- The Journal of neuroscience : the official journal of the Society for Neuroscience
- Published over 2 years ago
In the past, we showed that large electrolytic lesions of the dorsomedial hypothalamus (DMH) promoted hypothermia in cold-exposed restrained rats, but attenuated hypothermia in rats challenged with a high dose of bacterial lipopolysaccharide (LPS) in a thermogradient apparatus. The goal of this study was to identify the thermoeffector mechanisms and DMH representation of the two phenomena and, hence, understand how the same lesion could produce two opposite effects on body temperature. We found that the permissive effect of large electrolytic DMH lesions on cold-induced hypothermia was due to suppressed thermogenesis. DMH-lesioned rats also could not develop fever autonomically: they did not increase thermogenesis in response to a low, pyrogenic dose of LPS (10 μg/kg, i.v.). In contrast, changes in thermogenesis were uninvolved in the attenuation of the hypothermic response to a high, shock-inducing dose of LPS (5,000 μg/kg, i.v.); this attenuation was due to a blockade of cold-seeking behavior. To compile DMH maps for the autonomic cold defense and for the cold-seeking response to LPS, we studied rats with small thermal lesions in different parts of the DMH. Cold thermogenesis had the highest representation in the dorsal hypothalamic area. Cold seeking was represented by a site at the ventral border of the dorsomedial nucleus. Because LPS causes both fever and hypothermia, we originally thought that the DMH contained a single thermoregulatory site that worked as a fever-hypothermia switch. Instead, we have found two separate sites: one that drives thermogenesis, and the other, previously unknown, that drives inflammation-associated cold seeking.SIGNIFICANCE STATEMENTCold-seeking behavior is a life-saving response that occurs in severe systemic inflammation. We studied this behavior in rats with lesions in the dorsomedial hypothalamus (DMH) challenged with a shock-inducing dose of bacterial endotoxin. We built functional maps of the DMH and found the strongest representation of cold-seeking behavior at the ventral border of the dorsomedial nucleus. We also built maps for cold-induced thermogenesis in unanesthetized rats and found the dorsal hypothalamic area to be its main representation site. Our work identifies the neural substrate of cold-seeking behavior in systemic inflammation and expands the functional topography of the DMH – a structure that modulates autonomic, endocrine, and behavioral responses and is a potential therapeutic target in anxiety and panic disorders.
Esophageal Cooling Device Versus Other Temperature Modulation Devices for Therapeutic Normothermia in Subarachnoid and Intracranial Hemorrhage
- Therapeutic hypothermia and temperature management
- Published about 2 years ago
Achieving and maintaining normothermia (NT) after subarachnoid hemorrhage (SAH) or intracerebral hemorrhage (ICH) often require temperature modulating devices (TMD). Shivering is a common adverse effect of TMDs that can lead to further costs and complications. We evaluated an esophageal TMD, the EnsoETM (Attune Medical, Chicago, IL), to compare NT performance, shiver burden, and cost of shivering interventions with existing TMDs. Patients with SAH or ICH and refractory fever were treated with the EnsoETM. Patient demographics, temperature data, shiver severity, and amounts and costs of medications used for shiver management were prospectively collected. Controls who received other TMDs were matched for age, gender, and body surface area to EnsoETM recipients, and similar retrospective data were collected. All patients were mechanically ventilated. Fever burden was calculated as areas of curves of time spent above 37.5°C or 38°C. Demographics, temperature data, and costs of EnsoETM recipients were compared with recipients of other TMDs. Eight EnsoETM recipients and 24 controls between October 2015 and November 2016 were analyzed. There were no differences between the two groups in demographics or patient characteristics. No difference was found in temperature at initiation (38.7°C vs. 38.5°C, p = 0.4) and fever burden above 38°C (-0.44°C × hours vs. -0.53°C × hours, p = 0.47). EnsoETM recipients showed a nonsignificant trend in taking longer to achieve NT than other TMDs (5.4 hours vs. 2.9 hours, p = 0.07). EnsoETM recipients required fewer shiver interventions than controls (14 vs. 30, p = 0.02). EnsoETM recipients incurred fewer daily costs than controls ($124.27 vs. $232.76, p = 0.001). The EnsoETM achieved and maintained NT in SAH and ICH patients and was associated with less shivering and lower pharmaceutical costs than other TMDs. Further studies in larger populations are needed to determine the EnsoETM’s efficacy in comparison to other TMDs.
This study had 2 objectives: (1) to quantify the metabolic response to physical cooling in febrile patients with systemic inflammatory response syndrome (SIRS) and (2) to provide proof for the hypothesis that the efficiency of external cooling and the subsequent shivering response are influenced by site and temperature of surface cooling pads.
BACKGROUND: Induction of mild therapeutic hypothermia (TH; temperature 32-34°C) has become standard of care in many hospitals for comatose survivors of cardiac arrest. Pyrexia, or fever, is known to be detrimental in patients with neurologic injuries such as stroke or trauma. The incidence of pyrexia in the postrewarming phase of TH is unknown. We attempted to determine the incidence of fever after TH and hypothesized that those patients who were febrile after rewarming would have worse clinical outcomes than those who maintained normothermia in the postrewarming period. METHODS: Retrospective data analysis of survivors of out-of-hospital cardiac arrest (OHCA) over a period of 29 months (December 2007 to April 2010). Inclusion criteria: OHCA, age >18, return of spontaneous circulation, and treatment with TH. Exclusion criteria: traumatic arrest and pregnancy. Data collected included age, sex, neurologic outcome, mortality, and whether the patient developed fever (temperature > 100.4°F, 38°C) within 24 hours after being fully rewarmed to a normal core body temperature after TH. We used simple descriptive statistics and Fisher exact test to report our findings. RESULTS: A total of 149 patients were identified; of these, 82 (55%) underwent TH. The mean age of the TH cohort was 66 years, and 28 (31%) were female. In all, 54 patients survived for >24 hours after rewarming and were included in the analysis. Among the analyzed cohort, 28 (52%) of 54 developed fever within 24 hours after being rewarmed. Outcome measures included in-hospital mortality as well as neurologic outcome as defined by a dichotomized Cerebral Performance Category (CPC) score. When comparing neurologic outcomes between the groups, 16 (57%) of 28 in the postrewarming fever group had a poor outcome (CPC score 3-5), while 15 (58%) of 26 in the no-fever group had a favorable outcome (P = .62). In the fever group, 15 (52%) of 28 died, while in the no-fever group, 14 (54%) of 26 died (P = .62). CONCLUSION: Among a cohort of patients who underwent mild TH after OHCA, more than half of these patients developed pyrexia in the first 24 hours after rewarming. Although there were no significant differences in outcomes between febrile and nonfebrile patients identified in this study, these findings should be further evaluated in a larger cohort. Future investigations may be needed to determine whether postrewarming temperature management will improve the outcomes in this population.
This study investigated the effects of irrigation solutions, administered at either 21 or 37 °C in percutaneous nephrolithotomy (PCNL), on hypothermia and related postoperative complications such as late emergence and late recovery from anesthesia, shivering, lactic acidosis, and excess bleeding.
Induction of therapeutic hypothermia is often complicated by shivering. Nefopam, a nonsedative benzoxazocine analgesic, reduces the shivering threshold (triggering core temperature) with minimal side effects. Consequently, nefopam is an attractive drug for inducing therapeutic hypothermia. However, nefopam alone is insufficient and thus needs to be combined with another drug. Meperidine also reduces the shivering threshold. We therefore determined whether the combination of nefopam and meperidine is additive, infra-additive, or synergistic on the shivering threshold.
Prior studies suggest hypothermia may be beneficial in acute respiratory distress syndrome, but cooling causes shivering and increases metabolism. The objective of this study was to assess the feasibility of performing a randomized clinical trial of hypothermia in patients with acute respiratory distress syndrome receiving treatment with neuromuscular blockade because they cannot shiver.
- Therapeutic hypothermia and temperature management
- Published over 2 years ago
Targeted temperature management (TTM) has been recognized to protect tissue function and positively influence neurological outcomes after brain injury. While shivering during hypothermia nullifies the beneficial effect of TTM, traditionally, antishivering drugs or paralyzing agents have been used to reduce the shivering. The hypothalamic area of the brain helps in controlling cerebral temperature and body temperature through interactions between different brain areas. Thus, modulation of different brain areas either pharmacologically or by electrical stimulation may contribute in TTM; although, very few studies have shown that TTM might be achieved by activation and inhibition of neurons in the hypothalamic region. Recent studies have investigated potential pharmacological methods of inducing hypothermia for TTM by aiming to maintain the TTM and reduce the shivering effect without using antiparalytic drugs. Better survival and neurological outcome after brain injury have been reported after pharmacologically induced TTM. This review discusses the mechanisms and modulation of the hypothalamus with other brain areas that are involved in inducing hypothermia through which TTM may be achieved and provides therapeutic strategies for TTM after brain injury.
- South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde
- Published about 2 years ago
The electrocardiographic changes of hypothermia are discussed in this case of a man who was brought to an emergency centre with altered mental status. The main ECG signs are a shivering artefact baseline, J waves, and PR-, QRS- and QT-interval prolongation.