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- Therapeutic Hypothermia in Children and Adults with Severe Traumatic Brain Injury. [REVIEW]
- Ther Hypothermia Temp Manag 2014 Mar 1; 4(1):10-20.
Great expectations have been raised about neuroprotection of therapeutic hypothermia in patients with traumatic brain injury (TBI) by analogy with its effects after heart arrest, neonatal asphyxia, and drowning in cold water. The aim of this study is to review our present knowledge of the effect of therapeutic hypothermia on outcome in children and adults with severe TBI. A literature search for relevant articles in English published from year 2000 up to December 2013 found 19 studies. No signs of improvement in outcome from hypothermia were seen in the five pediatric studies. Varied results were reported in 14 studies on adult patients, 2 of which reported a tendency of higher mortality and worse neurological outcome, 4 reported lower mortality, and 9 reported favorable neurological outcome with hypothermia. The quality of several trials was low. The best-performed randomized studies showed no improvement in outcome by hypothermia-some even indicated worse outcome. TBI patients may suffer from hypothermia-induced pulmonary and coagulation side effects, from side effects of vasopressors when re-establishing the hypothermia-induced lowered blood pressure, and from a rebound increase in intracranial pressure (ICP) during and after rewarming. The difference between body temperature and temperature set by the biological thermostat may cause stress-induced worsening of the circulation and oxygenation in injured areas of the brain. These mechanisms may counteract neuroprotective effects of therapeutic hypothermia. We conclude that we still lack scientific support as a first-tier therapy for the use of therapeutic hypothermia in TBI patients for both adults and children, but it may still be an option as a second-tier therapy for refractory intracranial hypertension.
- The liver proteome in hibernating ground squirrels is dominated by metabolic changes associated with the long winter fast. [JOURNAL ARTICLE]
- Physiol Genomics 2014 Mar 18.
Small-bodied hibernators partition the year between active homeothermy and hibernating heterothermy accompanied by fasting. To define molecular events underlying hibernation that are both dependent and independent of fasting, we analyzed the liver proteome among two active and four hibernation states in 13-lined ground squirrels. We also examined fall animals transitioning between fed homeothermy and fasting heterothermy. Significantly enriched pathways differing between activity and hibernation were biased towards metabolic enzymes, concordant with the fuel shifts accompanying fasting physiology. Although metabolic reprogramming to support fasting dominated these data, arousing (rewarming) animals had the most distinct proteome among the hibernation states. Instead of a dominant metabolic enzyme signature, torpor-arousal cycles featured differences in plasma proteins and intracellular membrane traffic and its regulation. Phosphorylated NSFL1C, a membrane regulator, exhibited this torpor-arousal cycle pattern; its role in autophagosome formation may promote utilization of local substrates upon metabolic reactivation in arousal. Fall animals transitioning to hibernation lagged in their proteomic adjustment, indicating that the liver is more responsive than preparatory to the metabolic reprogramming of hibernation. Specifically, torpor use had little impact on the fall liver proteome, consistent with a dominant role of nutritional status. In contrast to our prediction of reprogramming the transition between activity and hibernation by gene expression, and then within-hibernation transitions by posttranslational modification (PTM), we found extremely limited evidence of reversible PTMs within torpor-arousal cycles. Rather, acetylation contributed to seasonal differences, being highest in winter (specifically in torpor), consistent with fasting physiology and decreased abundance of the mitochondrial deacetylase, SIRT3.
- [ABC ahead of rewarming in the treatment of accidental hypothermia.] [JOURNAL ARTICLE]
- Ugeskr Laeger 2014 Jan 6; 176(1):64-67.
The treatment of accidental hypothermia is still controversial and is missing detailed evidence-based guidelines. Current knowledge suggests that advanced trauma life support principles must be prioritized ahead of rewarming. In case of cardiac arrest, initiation of extracorporeal circulation before rewarming and prolongation of hypothermia at 33 °C to reduce reperfusion injury and cerebral hyperthermia is recommended but is not as yet implemented as standard treatment. We propose a simplified clinical approach to on-site triage of hypothermia: 1. Awake below 35 °C (Glasgow Coma Scale > 8). 2. Unconscious below 32 °C. 3. Absent respiration and circulation below 32 °C.
- [Long-term use of an endovascular temperature catheter.] [JOURNAL ARTICLE]
- Med Klin Intensivmed Notfmed 2014 Mar 12.
A patient suffering from severe cutaneous graft versus host disease (GvHD) developed generalized epidermolysis and refractory hypothermia. Due to the insufficient effect of traditional rewarming methods, an endovascular temperature catheter was placed via the femoral vein to achieve and maintain normothermia over a period of 31 days. This case shows that an endovascular temperature modulation device primarily made for short-term use may be safe and effective even over weeks and may offer an alternative to other rewarming methods in patients with severe epidermolysis and burns.
- Serotonin syndrome after therapeutic hypothermia for cardiac arrest: A case series. [JOURNAL ARTICLE]
- Resuscitation 2014 Mar 12.
To describe causes, manifestations, and diagnosis of serotonin syndrome following therapeutic hypothermia (TH) after cardiac arrest.Retrospective case series from a tertiary academic medical center.Three male patients suffered witnessed out-of-hospital cardiac arrests and were treated with induced TH. Initial cardiac rhythms included asystole in two and ventricular fibrillation in one. Following completion of rewarming, all three developed neurological signs unexpected for their clinical condition. These included rigidity, hyperreflexia, diffuse tremors, ankle clonus, and marked agitated delirium. Patients also were febrile, hypertensive, and tachycardic. A diagnosis of serotonin syndrome was made in all cases and serotonergic medications were discontinued. All three patients recovered consciousness and two made a full neurological recovery. One patient remained dependent on others for activities of daily living at the time of hospital discharge because of short-term memory impairment.Unexpected neurologic findings and prolonged high fever following recovery from TH can be manifestations of serotonin syndrome rather than post-cardiac arrest anoxic brain injury.
- The myocardial function during and after whole-body therapeutic hypothermia for hypoxic-ischemic encephalopathy, a cohort study. [Journal Article]
- Early Hum Dev 2014 May; 90(5):247-52.
Therapeutic hypothermia has become standard treatment for moderate and severe neonatal hypoxic-ischemic encephalopathy (HIE) to reduce cerebral morbidity and mortality. The effect on the heart is incompletely explored.To assess the myocardial function during and after whole-body therapeutic hypothermia for HIE.Observational cohort study.Forty-four infants with HIE cooled for 72hours were compared with 48 healthy term infants and 20 normothermic infants with HIE.Tissue Doppler deformation indices of myocardial function (peak systolic strain, peak systolic strain-rate, early diastole strain-rate and strain-rate in atrial systole) during (days 1 and 3) and after (day 4) therapeutic hypothermia.On days one and three all indices in both HIE groups were lower than the corresponding indices in the healthy infants. The two HIE groups had similar indices, except peak systolic strain-rate on days 1 and 3 and strain-rate in atrial systole on day 1. All strain-rate indices improved from day 3 to 4 (after rewarming) in the cooled group and achieved similar values to those in healthy infants on day 3. All indices were higher in the cooling-group after rewarming than in the normothermic infants with HIE on day 3, except early diastolic strain-rate.Infants with HIE had similarly impaired myocardial function during days 1-3 whether normothermic or hypothermic. The myocardial function improved significantly at day 4 (after rewarming), approaching the day 3 levels in the healthy neonates.
- Concentrations of remifentanil, propofol, fentanyl, and midazolam during rewarming from therapeutic hypothermia. [JOURNAL ARTICLE]
- Acta Anaesthesiol Scand 2014 Mar 11.
The clearance of sedatives and analgesics may be reduced by therapeutic hypothermia. However, little is known about the concentrations of such drugs during rewarming. The aim of this study was to describe the serum concentrations of sedatives and analgesics during rewarming from therapeutic hypothermia.Blood samples were collected for quantification of drug concentrations in 22 patients given analgesia/sedation with either remifentanil/propofol or fentanyl/midazolam during rewarming from therapeutic hypothermia (33-34°C) after cardiac arrest. Samples for were drawn before (-2 h) and during rewarming (0-8 h). Linear mixed effects models were used to describe serum concentrations and adjust for rates of infusion during rewarming from therapeutic hypothermia.Subjects with samples analyzed were remifentanil (n = 8), propofol (n = 14), fentanyl (n = 8), and midazolam (n = 8). Age, body mass index, and simplified acute physiology score II [mean (standard deviation)] were 64 (14.2) years, 27.3 (3.7) kg/m(2) , and 69 (13.2), respectively. While the concentration of fentanyl was not significantly affected by temperature, concentrations of remifentanil, propofol, and midazolam decreased with core temperature by 16%, 12%, and 11% (mean values) from 33°C to 37°C after adjusting for rates of infusion, respectively.Concentrations of remifentanil, propofol, and midazolam decreased during rewarming from therapeutic hypothermia when adjusting for rates of infusion. No changes were demonstrated for fentanyl.
- Coagulopathy induced by acidosis, hypothermia and hypocalcaemia in severe bleeding. [JOURNAL ARTICLE]
- Minerva Anestesiol 2014 Mar 7.
Acidosis, hypothermia and hypocalcaemia are determinants for morbidity and mortality during massive haemorrhages. However, precise pathological mechanisms of these environmental factors and their potential additive or synergistic anticoagulant and/or antiplatelet effects are not fully elucidated and are at least in part controversial. Best available evidences from experimental trials indicate that acidosis and hypothermia progressively impair platelet aggregability and clot formation. Considering the cellbased model of coagulation physiology, hypothermia predominantly prolongs the initiation phase, while acidosis prolongs the propagation phase of thrombin generation. Acidosis increases fibrinogen breakdown while hypothermia impairs its synthesis. Acidosis and hypothermia have additive effects. The effect of hypocalcaemia on coagulopathy is less investigated but it appears that below the cutoff of 0.9 mmol/L, several enzymatic steps in the plasmatic coagulation system are blocked while above that cutoff effects remain without clinical sequalae. The impact of environmental factor on haemostasis is underestimated in clinical practice due to our current practice of using routine coagulation laboratory tests such as partial thromboplastin time or prothrombin time, which are performed at standardized test temperature, after pH correction, and upon recalcification. Temperature-adjustments are feasible in viscoelastic point-of-care tests such as thrombelastography and thromboelastometry which may permit quantification of hypothermia-induced coagulopathy. Rewarming hypothermic bleeding patients is highly recommended because it improves patient outcome. Despite the absence of high-quality evidence, calcium supplementation is clinical routine in bleeding management. Buffer administration may not reverse acidosis-induced coagulopathy but may be essential for the efficacy of coagulation factor concentrates such as recombinant activated factor VII.
- Hypothermia-induced acute kidney injury in an elderly patient. [Journal Article]
- Korean J Intern Med 2014 Jan; 29(1):111-5.
Hypothermia, defined as an unintentional decline in the core body temperature to below 35℃, is a life-threatening condition. Patients with malnutrition and diabetes mellitus as well as those of advanced age are at high risk for accidental hypothermia. Due to the high mortality rates of accidental hypothermia, proper management is critical for the wellbeing of patients. Accidental hypothermia was reported to be associated with acute kidney injury (AKI) in over 40% of cases. Although the pathogenesis remains to be elucidated, vasoconstriction and ischemia in the kidney were considered to be the main mechanisms involved. Cases of AKI associated with hypothermia have been reported worldwide, but there have been few reports of hypothermia-induced AKI in Korea. Here, we present a case of hypothermia-induced AKI that was treated successfully with rewarming and supportive care.
- Cold-induced vasoconstriction may persist long after cooling ends: an evaluation of multiple cryotherapy units. [JOURNAL ARTICLE]
- Knee Surg Sports Traumatol Arthrosc 2014 Feb 23.
Localized cooling is widely used in treating soft tissue injuries by modulating swelling, pain, and inflammation. One of the primary outcomes of localized cooling is vasoconstriction within the underlying skin. It is thought that in some instances, cryotherapy may be causative of tissue necrosis and neuropathy via cold-induced ischaemia leading to nonfreezing cold injury (NFCI). The purpose of this study is to quantify the magnitude and persistence of vasoconstriction associated with cryotherapy.Data are presented from testing with four different FDA approved cryotherapy devices. Blood perfusion and skin temperature were measured at multiple anatomical sites during baseline, active cooling, and passive rewarming periods.Local cutaneous blood perfusion was depressed in response to cooling the skin surface with all devices, including the DonJoy (DJO, p = 2.6 × 10(-8)), Polar Care 300 (PC300, p = 1.1 × 10(-3)), Polar Care 500 Lite (PC500L, p = 0.010), and DeRoyal T505 (DR505, p = 0.016). During the rewarming period, parasitic heat gain from the underlying tissues and the environment resulted in increased temperatures of the skin and pad for all devices, but blood perfusion did not change significantly, DJO (n.s.), PC300 (n.s.), PC500L (n.s.), and DR505 (n.s.).The results demonstrate that cryotherapy can create a deep state of vasoconstriction in the local area of treatment. In the absence of independent stimulation, the condition of reduced blood flow persists long after cooling is stopped and local temperatures have rewarmed towards the normal range, indicating that the maintenance of vasoconstriction is not directly dependent on the continuing existence of a cold state. The depressed blood flow may dispose tissue to NFCI.