Prophylactic Hypothermia Research Articles

Alopecia prevention during chemotherapy: from the benchmark to real clinical practice. A prospective study

Background. Alopecia is one of the main side effects of anticancer chemotherapy and has a significant impact on patients’ appearance, quality of life, social adaptation and mental health of cancer patients. Estimated number of new cancer diagnosis increases annually alongside with the proportion of patients receiving chemotherapy. That means an annual increase in the global burden of chemo-induced alopecia and associated negative consequences. The development of various methods for the prevention of alopecia in cancer patients has continued for decades. However, convincing data have been obtained only for the scalp hypothermia method. In this point, the Paxman company’s cooling systems (UK) – the Orbis and Orbis II devices – have been most widely studied. Despite the fact that Orbis devices were approved in Russia more than 10 years ago, since then just a small amount of real clinical practice has been accumulated and questions regarding the effectiveness of scalp hypothermia in patients with variable cancers still remain open.
 Aim. Analysis of local clinical practice with scalp hypothermia via the Orbis II device for the prevention of alopecia in patients receiving various chemotherapy regimens.
 Materials and methods. An open, prospective, single-center study included patients with various cancer types who were indicated for chemotherapy. Orbis II device was used for prophylactic hypothermia. The severity of alopecia was assessed according to the CTCAE version 5.0 at baseline and during anticancer therapy.
 Results. From June 2022 to May 2023, scalp cooling procedures were performed in 51 patients, of them 78% of all procedures were performed in female cancers: breast tumors – 109 (52.2%) procedures, ovarian cancer– 33 (15.8%), and cervix cancer – 22 (10.5%). The effectiveness of scalp hypothermia in preventing of severe alopecia was 73%.
 Conclusion. Scalp cooling can be considered as an effective method for the prevention of chemotherapy induced alopecia. Further studies are needed to assess larger patient populations to identify favorable and negative factors that affect potency of the hypothermia.

Association Between Early External Ventricular Drain Insertion and Functional Outcomes 6 Months Following Moderate-to-Severe Traumatic Brain Injury.

Traumatic brain injury (TBI) is a leading global cause of morbidity and mortality. Intracranial hypertension following moderate-to-severe TBI (m-sTBI) is a potentially modifiable secondary cerebral insult and one of the central therapeutic targets of contemporary neurocritical care. External ventricular drain (EVD) insertion is a common therapeutic intervention used to control intracranial hypertension and attenuate secondary brain injury. However, the optimal timing of EVD insertion in the setting of m-sTBI is uncertain and practice variation is widespread. Therefore, we aimed to assess if there is an association between timing of EVD placement and functional neurological outcome at 6 months post m-sTBI. We pooled individual patient data for all relevant harmonizable variables from the Erythropoietin in Traumatic Brain Injury (EPO-TBI) and Prophylactic Hypothermia Trial to Lessen Traumatic Brain Injury (POLAR) randomized control trials, and the Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) Core Study version 3.0 and Australia-Europe NeuroTrauma Effectiveness Research in TBI (Oz-ENTER) prospective observational studies to create a combined dataset. The Glasgow Coma Scale (GCS) score was used to define TBI severity and we included all patients admitted to an intensive care unit with a GCS ≤12, who were 15 years or older and underwent EVD placement within 7 days of injury. We used hierarchical multi-variable logistic regression models to study the association between EVD insertion within 24 h of injury (early) compared with EVD insertion more than 24 h after injury (late) and 6-month functional neurological outcome measured using the Glasgow Outcome Score Extended (GOSE). In total, 2536 patients were assessed. Of these, 502 (20%) underwent early EVD insertion and 145 (6%) underwent late EVD insertion. Following adjustment for the IMPACT (International Mission for Prognosis and Analysis of Clinical Trials in TBI) score extended (Core + CT), sex, injury severity score, study and treatment site, patients receiving a late EVD had higher odds of death or severe disability (GOSE 1-4) at 6 months follow-up than those receiving an early EVD adjusted odds ratio; 95% confidence interval, 2.14; 1.22-3.76; p = 0.008. Our study suggests that in patients with m-sTBI where an EVD is needed, early (≤ 24 h post-injury) insertion may result in better long-term functional outcomes. This finding supports future prospective investigation in this area.

Overview of Hypothermia, Its Role in Neuroprotection, and the Application of Prophylactic Hypothermia in Traumatic Brain Injury.

The current standard of practice is to maintain normothermia in traumatic brain injury (TBI) patients despite the theoretical benefits of hypothermia and numerous animal studies with promising results. While targeted temperature management or induced hypothermia to support neurological function is recommended for a select patient population postcardiac arrest, similar guidelines have not been instituted for TBI. In this review, we will examine the pathophysiology of TBI and discuss the benefits and risks of induced hypothermia in this patient population. In addition, we provide an overview of the largest randomized controlled trials testing-induced hypothermia. Our literature review on hypothermia returned a myriad of studies and trials, many of which have inconclusive results. The aim of this review was to recognize the effects of hypothermia, summarize the latest trials, address the inconsistencies, and discuss future directions for the study of hypothermia in TBI.

Measured energy expenditure in mildly hypothermic critically ill patients with traumatic brain injury: A sub-study of a randomized controlled trial

Prophylactic hypothermia, often used in critically ill patients with traumatic brain injury, reduces energy expenditure and may affect energy delivered by nutrition therapy. The primary objective of this study was to measure energy expenditure in hypothermic patients over the first 3 days after traumatic brain injury (TBI). Secondary objectives included comparison of measured energy expenditure and nutrition delivery to day 7. A prospective sub-study of a randomized controlled trial conducted in patients with severe TBI, investigating prophylactic hypothermia (33-35°C) as a neuroprotective therapy. In two centers, indirect calorimetry was initiated within 24h of randomization and repeated up to twice daily to day 7. Data are presented as n (%), mean (standard deviation (SD)), median [interquartile range (IQR)], and mean difference (95% confidence interval (CI)). Forty patients were included (20 in each group), with 17 patients in the hypothermic and 16 in the normothermic group having an indirect calorimetry measurement in the first 3 days. Over the first 3 days, the mean temperature in the hypothermic and normothermic groups was 33.5 (0.6) ºC (n=17) and 37 (0.5) ºC (n=16), p<0.0001, and the mean measured energy expenditure, was 21 (5) and 27 (4) kcal/kg, p=0.002, representing a mean difference of 5 (95% CI: 2-8) kcal/kg. Energy expenditure was 20% (95% CI: 9.5-29%) less in hypothermia patients compared to normothermia patients. Hypothermia patients also had higher gastric residual volumes across the 7 day study period (438 (237) mls vs 184 (103) mls, p<0.0001) and higher use of metoclopramide and erythromycin as prokinetics. Despite enteral nutrition intolerance, hypothermia patients received 93% of measured energy expenditure over 7 days. In TBI patients, energy expenditure was 20% less when receiving prophylactic hypothermia compared to normothermia. Greater gastric residual volumes, use of prokinetics and energy delivery that approximated measured energy expenditure was also observed in hypothermia patients. POLAR-RCT: clinicaltrials.gov Identifier: NCT00987688; Anzctr.org.au Identifier: ACTRN12609000764235. This sub-study was not registered separately.

Current Prophylactic Hypothermia for Intracranial Hypertension after Traumatic Brain Injury

Current Prophylactic Hypothermia for Intracranial Hypertension after Traumatic Brain Injury

Thromboelastography to Assess Coagulopathy in Traumatic Brain Injury Patients Undergoing Therapeutic Hypothermia.

Therapeutic hypothermia has been a treatment option for patients with severe traumatic brain injury (TBI) for many years. There has, however, been uncertainty whether hypothermia in this context also increased clinical bleeding risk, perhaps due to platelet dysfunction. Standard coagulation tests do not allow accurate assessment of in vivo coagulation. We studied specific coagulation abnormalities in patients undergoing therapeutic hypothermia for severe TBI using bedside thromboelastography (TEG).We studied 20 patients with severe blunt TBI from a single tertiary ICU who were enrolled in the prophylactic hypothermia to lessen traumatic brain injury (POLAR) trial. Ten patients had been randomized to hypothermia, and 10 were controls receiving normothermic standard care. TEG was undertaken during and after therapeutic hypothermia, and at the same time points in controls. Coagulation profiles were then compared between the hypothermic and control patients, and also between hypothermia and later normothermia in the study patients. Patients were primarily young (mean age 34 years) and male (85%). Measures of injury severity, including Glasgow coma score and injury severity scale, were not different between groups. Using TEG, the median alpha angle was reduced in hypothermic patients compared with controls (69.2° vs. 72.0°, p = 0.02), although both were within the normal range. LY30 was also reduced (0.0% vs. 0.5%, p < 0.01). Both differences persisted when hypothermic patients were compared with themselves during later normothermia. Therapeutic hypothermia during severe TBI causes a small decrease in the rate of clot formation. However, this decrease is within the normal range, and is unlikely to be clinically significant.

The Effect of Prophylactic Hypothermia on Neurophysiological and Functional Measures in the Setting of Iatrogenic Spinal Cord Impact Injury

Iatrogenic spinal cord injury (iSCI) during spinal corrective surgery can result in devastating complications, such as paraplegia or paraparesis. Perioperatively, iSCI often occurs as a direct injury during spinal cord instrumentation placement. Currently, treatment of iSCI remains limited to posttraumatic hypothermia, which has demonstrated some value in recent clinical trials. Here we report the outcomes of preinjury hypothermia initiated preprocedurally and maintained for a considerable time after iSCI. Twenty-six female Sprague-Dawley rats were assigned at random to either a normothermic group (36 °C) or a hypothermic group (32 °C) and then underwent a laminectomy procedure at the T8 level. Each group was further divided at random to receive a 200-kdyn force contusive spinal cord injury or a sham impact. Hypothermic rats were then rewarmed after 2 hours of hypothermic treatment. Behavioral scores, temperature profiles, weights, and somatosensory evoked potentials were obtained at baseline and at specified time points after the procedure. The median survival was 42 days for the iSCI hypothermic group and 11 days for the iSCI normothermic group (hazard ratio, 3.82; 95% confidence interval, 1.52-9.57). The probability of survival was significantly higher in the iSCI hypothermic group compared with the iSCI normothermic group (χ2= 4.18; P= 0.040). The hypothermic group exhibited a higher Basso, Beattie and Bresnahan (BBB) locomotor rating scale score (17 vs. 14; P < 0.01), lower normalized latencies (1.06 ± 0.16 seconds vs. 1.34 ± 0.17 seconds; P= 0.04), and higher peak-to-peak amplitudes (0.32 ± 0.10 μV vs. 0.12 ± 0.09 μV; P= 0.005). The use of prophylactic hypothermia before iSCI was significantly associated with an increased survival rate, higher BBB scores, and improved neurophysiological measures.

Early Prophylactic Hypothermia for Patients With Severe Traumatic Injury: Premature to Close the Case.

Early Prophylactic Hypothermia for Patients With Severe Traumatic Injury: Premature to Close the Case.

Patients with Traumatic Brain Injury Do Not Benefit from Prophylactic Hypothermia, Large Study Finds

Patients with Traumatic Brain Injury Do Not Benefit from Prophylactic Hypothermia, Large Study Finds

Effect of Early Sustained Prophylactic Hypothermia on Neurologic Outcomes Among Patients With Severe Traumatic Brain Injury

After severe traumatic brain injury, induction of prophylactic hypothermia has been suggested to be neuroprotective and improve long-term neurologic outcomes. To determine the effectiveness of early prophylactic hypothermia compared with normothermic management of patients after severe traumatic brain injury. The Prophylactic Hypothermia Trial to Lessen Traumatic Brain Injury-Randomized Clinical Trial (POLAR-RCT) was a multicenter randomized trial in 6 countries that recruited 511 patients both out-of-hospital and in emergency departments after severe traumatic brain injury. The first patient was enrolled on December 5, 2010, and the last on November 10, 2017. The final date of follow-up was May 15, 2018. There were 266 patients randomized to the prophylactic hypothermia group and 245 to normothermic management. Prophylactic hypothermia targeted the early induction of hypothermia (33°C-35°C) for at least 72 hours and up to 7 days if intracranial pressures were elevated, followed by gradual rewarming. Normothermia targeted 37°C, using surface-cooling wraps when required. Temperature was managed in both groups for 7 days. All other care was at the discretion of the treating physician. The primary outcome was favorable neurologic outcomes or independent living (Glasgow Outcome Scale-Extended score, 5-8 [scale range, 1-8]) obtained by blinded assessors 6 months after injury. Among 511 patients who were randomized, 500 provided ongoing consent (mean age, 34.5 years [SD, 13.4]; 402 men [80.2%]) and 466 completed the primary outcome evaluation. Hypothermia was initiated rapidly after injury (median, 1.8 hours [IQR, 1.0-2.7 hours]) and rewarming occurred slowly (median, 22.5 hours [IQR, 16-27 hours]). Favorable outcomes (Glasgow Outcome Scale-Extended score, 5-8) at 6 months occurred in 117 patients (48.8%) in the hypothermia group and 111 (49.1%) in the normothermia group (risk difference, 0.4% [95% CI, -9.4% to 8.7%]; relative risk with hypothermia, 0.99 [95% CI, 0.82-1.19]; P = .94). In the hypothermia and normothermia groups, the rates of pneumonia were 55.0% vs 51.3%, respectively, and rates of increased intracranial bleeding were 18.1% vs 15.4%, respectively. Among patients with severe traumatic brain injury, early prophylactic hypothermia compared with normothermia did not improve neurologic outcomes at 6 months. These findings do not support the use of early prophylactic hypothermia for patients with severe traumatic brain injury. clinicaltrials.gov Identifier: NCT00987688; Anzctr.org.au Identifier: ACTRN12609000764235.

Statistical analysis plan for the POLAR-RCT: The Prophylactic hypOthermia trial to Lessen trAumatic bRain injury-Randomised Controlled Trial

BackgroundThe Prophylactic hypOthermia to Lessen trAumatic bRain injury-Randomised Controlled Trial (POLAR-RCT) will evaluate whether early and sustained prophylactic hypothermia delivered to patients with severe traumatic brain injury improves patient-centred outcomes.MethodsThe POLAR-RCT is a multicentre, randomised, parallel group, phase III trial of early, prophylactic cooling in critically ill patients with severe traumatic brain injury, conducted in Australia, New Zealand, France, Switzerland, Saudi Arabia and Qatar. A total of 511 patients aged 18–60 years have been enrolled with severe acute traumatic brain injury.The trial intervention of early and sustained prophylactic hypothermia to 33 °C for 72 h will be compared to standard normothermia maintained at a core temperature of 37 °C.The primary outcome is the proportion of favourable neurological outcomes, comprising good recovery or moderate disability, observed at six months following randomisation utilising a midpoint dichotomisation of the Extended Glasgow Outcome Scale (GOSE). Secondary outcomes, also assessed at six months following randomisation, include the probability of an equal or greater GOSE level, mortality, the proportions of patients with haemorrhage or infection, as well as assessment of quality of life and health economic outcomes. The planned sample size will allow 80% power to detect a 30% relative risk increase from 50% to 65% (equivalent to a 15% absolute risk increase) in favourable neurological outcome at a two-sided alpha of 0.05.DiscussionConsistent with international guidelines, a detailed and prospective analysis plan has been developed for the POLAR-RCT. This plan specifies the statistical models for evaluation of primary and secondary outcomes, as well as defining covariates for adjusted analyses and methods for exploratory analyses. Application of this statistical analysis plan to the forthcoming POLAR-RCT trial will facilitate unbiased analyses of these important clinical data.Trial registrationClinicalTrials.gov, NCT00987688 (first posted 1 October 2009); Australian New Zealand Clinical Trials Registry, ACTRN12609000764235. Registered on 3 September 2009.

Prophylactic and Therapeutic Hypothermia in Severe Traumatic Brain Injury

This review aims to synthesize knowledge on the efficacy and safety of prophylactic hypothermia (PH—cooling started shortly after trauma) and therapeutic hypothermia (TH—cooling started to treat increased intracranial pressure (ICP)) in severe traumatic brain injury (TBI). Current evidence on the use of hypothermia in severe TBI is conflicting. Recent multicenter trials on the topic have demonstrated no improvement in functional outcome or mortality in patients treated with PH. Certain patient subgroups seem to benefit from this therapy, such as individuals undergoing craniotomy. TH appears to be ineffective as a stage 2 therapy, but evidence supports its use in stage 3 ICP management. Higher risks of complications occur with hypothermia, but they can be mitigated by using milder cooling, selective brain cooling, and gradual rewarming. Short-term PH appears to be ineffective in improving outcome for severe TBI. However, PH may still be useful as a longer-duration therapy and in specific patient subgroups. In addition, optimal rate of rewarming and ideal target temperature need to be established. TH as a stage 3 ICP control therapy has only shown benefit in small trials. Higher-quality studies that shed light on these questions are required.

Future Directions for Hypothermia following Severe Traumatic Brian Injury.

Traumatic brain injury (TBI) is a serious health care problem on both individual and public health levels. As a major cause of death and disability in the United States, it is associated with a significant economic and public health burden. Although the evidence to support the use of induced hypothermia on neurologic outcome after cardiac arrest is well established, its use in treating TBI remains controversial. Hypothermia has the potential to mitigate some of the destructive processes that occur as part of secondary brain injury after TBI. Hypothermia can be helpful in lowering intracranial pressure, for example, but its influence on functional outcome is unclear. There is insufficient evidence to support the broad use of prophylactic hypothermia for neuroprotection after TBI. Investigators are beginning to more carefully select patients for temperature modulating therapies, in a more personalized approach. Examples include targeting immunomodulation and scaling hypothermia to achieve metabolic targets. This review will summarize the clinical evidence for the use of hypothermia to limit secondary brain injury following acute TBI.

A randomized placebo-controlled trial of progesterone with or without hypothermia in patients with acute severe traumatic brain injury.

Among newer neuroprotectant modalities, hypothermia and progesterone have shown a beneficial role in preliminary studies enrolling patients with severe traumatic brain injury (sTBI). The primary objective of this study was to evaluate the efficacy of progesterone with or without prophylactic hypothermia in acute sTBI patients. This is a prospective, outcome assessor, statistician blinded, randomized, and placebo-controlled phase II trial of progesterone with or without hypothermia (factorial design). All adult patients (18-65 years) with acute sTBI (Glasgow coma score of 4-8) and presenting to trauma center within 8 h after injury were included in the trial. Computer-generated randomization was done after exclusion; sequentially numbered, opaque, sealed envelope technique was used for allocation concealment. The enrollment duration was from January 2012 to October 2014. The primary endpoint was dichotomized Glasgow outcome score (GOS) [poor recovery = GOS 1-3; good recovery = GOS 4-5], and secondary endpoints were functional independence measure (FIM) score and mortality rate at 6 and 12 months follow-up after recruitment. A total of 107 patients were randomized into four groups (placebo [n = 27], progesterone [n = 26], hypothermia alone [n = 27], and progesterone + hypothermia [n = 27]). The study groups were comparable in baseline parameters except for a higher incidence of decompressive craniectomy in the placebo group (P = 0.001). The analysis of GOS at 6 months revealed statistically significant better outcome in the hypothermia group (82%; P = 0.01) and a weaker evidence for progesterone group (74%; P = 0.07) as compared with the placebo group (44%). However, the outcome benefit was marginal at 1-year follow-up for the hypothermia group (82% vs. 58%, P = 0.17). The adjusted odds ratio of poor recovery at 6 months in the hypothermia group was 0.21 (confidence interval = 0.05-0.84, P = 0.03), as compared with the placebo group. Although mean FIM scores at 6 and 12 months respectively were marginally higher in the hypothermia and progesterone groups compared with the placebo group (P = 0.06 and 0.27), the proportion of functionally independent individuals were similar in all the groups (P = 0.79 and 0.51). The mortality rates were similar in all the groups at 6 and 12 months (P = 0.78 and 0.52 respectively). A strong evidence for prophylactic hypothermia and a weak evidence for progesterone therapy was observed for a better primary outcome at 6 months as compared to the placebo. A similar trend was observed at a 1-year follow-up. Contrary to our hypothesis, prophylactic hypothermia therapy suppressed the beneficial effects of progesterone therapy in sTBI patients. The complex cascades of factors responsible for such interactions are still unknown and need to be further determined.

Traumatic Brain Injury: Treatment with Mild Prolonged Hypothermia

Introduction: Hypothermia has been used as a method of brain protection in patients with traumatic brain injury (TBI) for many years. The protective effects of hypothermia are related to the inhibition of the excitatory amino acids (EAA) release including glutamate. The hypothermic decline of the cerebral metabolic rate of oxygen is also another mechanism of brain protection because it maintains the aerobic metabolism of the brain. Aim of the work: To study the effect of mild hypothermia on the outcome and complications in severe head trauma. Patients and methods: Ninety four patients (16-60 years old) with severe head trauma (Glasgow coma scale ≤ 8) were classified into hypothermic group (n=47) and normothermic group (n=47). The jugular venous bulb oxygen saturation, the jugular venous lactate, the Glasgow outcome scale at hospital discharge (GOS-HD), the length of ICU stay and other variables were measured and recorded. Results: Mild hypothermia improved the jugular venous bulb oxygen saturation, decreased the jugular venous lactate, with no effect on (GOS-HD). Conclusion: Prophylactic mild hypothermia lacks any effect on the outcome in patients with TBI, although there is improvement in the cerebral oxygenation and decrease the oxygen extraction and prevention of the anaerobic metabolism by decreasing the level of serum lactate. A subgroup of patients with intracranial hematoma may benefit from this type of treatment.

Long-term results in patients with intracranial aneurismal subarachnoid hemorrhages and their prognosis.

In 260 patients with intracranial aneurism hemorrhages long-term results were estimated according to Rankin scale 2,5 years after operation. Long-term results by Rankin 0-2 were considered to be “good”, 3-5 were considered to be “bad” ones. Two years after operation 53% of all patients had “good” long-term outcome. Factors negatively influencing long-term outcomes are to be the following: intra-operational aneurism rupture, temporary arterial clipping in the process of operation, complications in the post-operational period, angiospasm according to the transcranial Doppler sonography, angiospasm prevalence, clinicopathologic hemorrhage characteristics “subarachnoid hemorrhage+others”, critical condition according to H-H&gt;1, feminine sex, aneurism location in the forebrain arteria, subarachnoid hemorrhage lesion according to Fisher&gt; II, ischemic heart disease, pathological comorbitidy, ABO blood group – III or IV. “Good” treatment results 2,5 years after treatment are prognosticated in patients with severe invalidity by Glasgo scale (GOS=3) on hospital discharge, in those who didn’t experience ischemic stroke after operation and with severity of condition I or II according to H-H on admission. In patients with GOS-3 on hospital discharge the best long-term results according to Rankin were observed in those treated under hypothermia conditions. Hypertensive disease worsens long-term results according to Rankin even in patients with GOS-5 on hospital discharge. With positive renovation results by Rankin 0 or 1 in the post-operation period (GOS = 5) excellent long-term results are prognosticated, but the best results could be obtained in patients without hypertensive disease under prophylactic hypothermia.

Protocol for a multicentre randomised controlled trial of early and sustained prophylactic hypothermia in the management of traumatic brain injury

Protocol for a multicentre randomised controlled trial of early and sustained prophylactic hypothermia in the management of traumatic brain injury

Glycemia in conditions of hypothermia in patients with intracranial aneurysmal hemorrhage

Despite the proven effectiveness of hypothermia as a method of neuroprotection, the presence of significant side effects requires further development of detailed protocols of usage, especially glucose. Aim: Improving treatment outcomes of patients with subarachnoid aneurysmal hemorrhage by preventing the development of hyperglycemia during systemic hypothermia. Materials and Methods: The study involved 48 patients with spontaneous subarachnoid hemorrhage of aneurysmal origin. All patients were conducted intracranial surgery - clipping aneurysms of cerebral vessels during regression of arterial vascular spasm (AVS) in the systemic hypothermia prevention. Therapeutic hypothermia was performed in 29 patients with complicated disease course for 48 hours. It is evaluated the effectiveness of its own method of prevention and correction of hyperglycemia - permanent short-acting insulin before the warm saline at a dose of 2 units/hour during hypothermia Results: During the prevention of hypothermia using methods of hyperglycemia episodes of above 10 mmol / L did not observe the rejection of a group of patients using the conventional method of correction of glycemia. Episodes of hypoglycemia do not observed in both groups of the study. Up to 48 hours of therapeutic hypothermia glucose levels remained stable, after 48 hours of hypothermia it is observed a significant increase in blood glucose that was cool termination criterion. Conclusions: Holding insulin infusion at short-acting dose of 2 units/hour during prophylactic hypothermia prevents episodes of hyperglycemia and consequently helps to maintain homeostasis. Carrying insulin infusion at short-acting dose of 2 units/hour during therapeutic hypothermia promotes stable blood glucose levels to 48 hours. After 48 hours of hypothermia in 51.72% of patients experienced a significant increase in blood glucose, which is one of the criteria for termination of cooling

Prophylactic hypothermia and neuromuscular blockade to limit myocardial oxygen demand in a critically anemic Jehovah's Witness after emergency surgery

Management of anemic patients refusing blood transfusion remains challenging. Concomitant coronary artery disease further complicates management. We sought to decrease the likelihood of cardiac events by employing hypothermia and neuromuscular blockade, in addition to limited phlebotomy, in a critically anemic Jehovah's Witness patient following emergent colectomy. The patient's hemoglobin concentrations were trended with serial blood gases. Neuromuscular blockade was instituted with cisatracurium, followed by hypothermia to a target of 32°C. The patient's lowest hemoglobin levels occurred on postoperative day 3 before beginning to rise. There were no postoperative cardiac events reported during the patient's course of stay. She recovered well with no evidence of anemia or cardiac events at 1-year follow-up. We conclude that targeted hypothermia with neuromuscular blockade, as an adjunct to accepted techniques, may be an alternative for critically anemic patients with coronary artery disease refusing blood transfusion.

Therapeutic hypothermia in traumatic brain injury

Hypothermia has profound effects on the brain function but importantly is potentially protective against both focal and global injuries. Aspects of the biochemical response to acute ischaemia and trauma, which are associated with poor outcome, can be inhibited by cooling. Unlike many pharmacological treatments that tend to antagonise a single neurochemical process, hypothermia offers a simple method of inhibiting multiple pathological processes simultaneously. It therefore has the potential, if applied correctly, to improve outcomes after acute brain injuries, where drug trials have so far failed. The systemic cooling of patients after acute brain injury is an established treatment modality in many neuro-ICUs. It is a strategy for protecting the injured brain that makes intuitive sense and can reduce both intracranial pressure and the potential for ischaemic secondary insults. Basic science evidence also suggests that cooling can attenuate many secondary biochemical cascades that are activated after acute injury. However, despite these multiple lines of supportive evidence there is as yet no confirmation from a high-quality randomised controlled trial that prophylactic hypothermia improves outcome or reduces mortality. This talk will look at the potentially beneficial effects of hypothermia on the biochemistry of acute brain injury, consider the reasons for the failure to demonstrate clinical efficacy and review the supportive data from meta-analysis, suggesting how hypothermia might be best delivered. Finally I will discuss EuroTherm3235, a European Society of Intensive Care Medicine funded multicentre randomised controlled trial investigating prophylactic hypothermia in traumatic brain injury, which draws on the lessons from the available literature.