Abstracts from the 3rd Annual Therapeutic Hypothermia and Temperature Management ConferenceMarch 4–5, 2013Miami, FL

Abstract

Therapeutic Hypothermia and Temperature ManagementVol. 3, No. 2 AbstractsFree AccessAbstracts from the 3rd Annual Therapeutic Hypothermia and Temperature Management ConferenceMarch 4–5, 2013Miami, FLPublished Online:14 Jun 2013https://doi.org/10.1089/ther.2013.1505AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail AbstractsAva M. Puccio University of Pittsburgh, Department of Neurosurgery, Pittsburgh, Pennsylvania.Fever Control in Traumatic Brain Injury: Nursing ConsiderationsFever, a component of secondary injury, is a risk factor for decreased neurological outcome, mortality and longer length of stays in the traumatic brain injury population, as well as the general neurologic ICU population. Fever remains a high occurrence (73%) with multiple and extended febrile episodes. The goal of the critical care team is to minimize secondary injury. The threshold for initial fever management is usually set high, at 38.3–38.5°C, although it has been shown that brain temperature is often 1 ½ times higher than bladder temperature. Conventional surface cooling, with cooling blankets, has been shown to be ineffective by limiting the access in the multi-trauma patient, who may have less surface area to cool with abdominal trauma and/or extremity fractures. It is more nursing time intensive with limited temperature precision (peaks and valleys). Controlled normothermia assists fever prophylaxis by having a temperature set-point that is driven by newer technology (either surface energy transfer cooling pads or intravascular cooling catheters). These allow more accurate temperature management and are less time consuming for the nursing staff. However, the use of either system has nuances associated with them. Energy transfer pads are more precise than traditional surface cooling, but nursing considerations for assessing skin integrity remains, especially in patients with poor perfusion. Shivering is a concern and needs to be managed with sedation to avoid increased intracranial pressure and metabolic demands. Intravascular cooling is an option in the ICU patient who requires a central line and may reduce shivering and skin concerns.Michael N. Diringer Washington University, St. Louis, Missouri.Maintaining Normothermia In Neuro Critical CareControl of body temperature involves a dynamic interaction with the environment and is managed by hypothalamic centers which are also influenced by exercise, emotions and endocrine function. Regulation of heat loss is controlled by redistribution of blood flow to or away from body surface and diaphoresis. Fever is a stereotyped adaptive response to infectious and inflammatory stimuli that may confer an immunological advantage to the host over invading microorganisms and involves a complex interplay of neuroendocrine, autonomic and behavioral responses. It is very common in the ICU affecting almost half of general ICU patients and is associated with higher mortality. Fever appears to be even more common in the Neuro ICU where over 90% of patients in the ICU for more than 2 weeks become febrile. The rationale for treating fever includes limiting the adverse effect of increased metabolic demand, sympathetic tone, oxygen consumption and minute ventilation, cognitive impairment and worsening of neurological deficits and LOC in patients with brain insults. It has been associated with worse outcome in numerous studies of head injury, stroke and intracerebral hemorrhage. Still fever appears to help fight infections; treatment with antipyretics prolongs the course of malaria and febrile patients with community acquired pneumonia have improved survival over afebrile patients. Approaches to treating fever include antipyretics, which are only effective in some cases, infusion of cooled solution, surface cooling devices and intravascular devices. The intravascular devices are the most effective at suppressing fever but also the most invasive. All methods, except antipyretics, can produce shivering which dramatically increases metabolic demand.Patrick M. Kochanek , Steven L. Shein , Vincent Vagni , Keri Feldman , Erik Brockman , Hülya Bayır , and Robert S.B. Clark Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine and Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania.Delayed Hyperthermia Exacerbates Neuronal Death and Neuroinflammation after Experimental Traumatic Brain InjuryHyperthermia (HT) has been shown to exacerbate damage after traumatic brain injury (TBI), however, the time interval during which exposure to HT exacerbates damage and the mechanism or mechanisms mediating this effect remain to be defined. We hypothesized that hippocampal neuronal death after TBI would be increased by HT in the initial 72 h after injury and that exacerbation of neuro-inflammation in the injured brain might mediate some of the detrimental effects. Anesthetized, normothermic C57BL6J adult male mice underwent TBI by controlled cortical impact (6 m/s, 1.2 mm). All injured mice underwent a single 2 h period of post-TBI temperature manipulation, with brain or temporalis muscle temperature targeted to 37°C (normothermia [NT]) or 39°C (HT) at 15 min, 24 h, 72 h or 96 h. We carried out four separate studies. In study 1, mice were divided into 7 groups: naïve (no TBI), 15NT, 15HT, 24NT, 24HT, 72HT and 96HT and temperature regulation was guided by a brain temperature probe. In study 2, we repeated study 1 using selected groups but titrated temperature using a temporalis muscle probe. In study 3, we delayed application of HT or NT to 7 d after TBI and allowed the mice to recover out to 21 d after injury. Finally, in study 4, we induced HT or NT at 24 h after TBI, and monitored macrophages in brain over the initial 7 d after injury using MPIO particles and magnetic resonance microscopy. In all studies, during temperature regulation, isoflurane and femoral catheters were used. Vital signs were recorded every 5 min and Lactated Ringer's (LR) given if MAP<70 mmHg. Mice were sacrificed 7 d or 21 d after TBI and brains stained with H&E. Macrophage accumulation in injured brain was assessed ex vivo in injured brain at 11.7 Tesla. We found that cell death in CA1 and CA3 hippocampus were increased by HT vs. NT when applied between 24 and 96 h after TBI. Early (15 min) and late (7 d) HT exposure did not exacerbate neuronal loss vs. NT. HT at 24 h after TBI doubled macrophage accumulation in the injured brain vs. NT. Our data suggest that brief exposure to a clinically relevant HT episode between 24 and 72 h after experimental TBI produces a marked exacerbation of neuronal death in CA1 and enhanced macrophage accumulation. Whether the increase in macrophage accumulation represents a key secondary injury mechanism or a response to HT-induced cell death remains to be determined. We speculate that meticulous temperature control and/or the use of targeted anti-inflammatory therapies may be important to reducing the burden of the secondary insult. Supported by HD040686, the Laerdal Foundation, and the Ann Thompson fellowship grant.Arie Blitz and Tina Blitz University Hospitals Case Medical Center, Cleveland, Ohio.Temperature Management and Cardiac SurgeryTemperature management is a topic that has been at the forefront of cardiac surgery for over 5 decades. In 1958 the preeminent cardiac surgeon Henry Swan wrote of the success of two important tools in cardiac surgery: “Both hypothermia and cardiopulmonary bypass (CPB) can now be said to be technics (sic) of proven merit.”(1). Over the ensuing years there have been several publications regarding the use of intraoperative hypothermia as an adjunct to CPB and the possible detrimental effect of postoperative hypothermia. Martin et al, in a prospective, randomized trial, found that the neurologic event rate was at least threefold higher in patients randomized to undergoing normothermic CPB as opposed to hypothermic CPB (2). Following publication of this study, numerous other studies led to conflicting results, most likely due to heterogeneity of populations and methodology amongst the studies.It has been well established that perioperative hypothermia is associated with worse outcomes in a variety of non-cardiac operations. Two large retrospective studies have examined the effect of postoperative hypothermia on outcomes after cardiac surgery. Insler and colleagues found that a bladder temperature of less than 36°C upon reaching the ICU after CABG was associated with a higher mortality rate on multivariate analysis (3). Karalapillai et al., using a large Australian ICU database, concluded that persistent hypothermia (>24 hrs) but not transient hypothermia (<24 hrs) was associated with a higher mortality rate after a variety of cardiac operations (4). Importantly, these studies do not necessarily imply a causal link between postoperative hypothermia and mortality. Numerous cases were presented illustrating the potential beneficial effect of temperature management using an intravascular catheter, both during and following cardiac surgery. These included cases where the warming mode was used, including aortic dissection repair, mechanical circulatory support, reoperative surgery, and flap surgery. Other cases were presented where cooling techniques may be of benefit. These include suspected or proven neurological injury, vasoplegia, and low cardiac output syndrome. Emphasis was placed on the fact that, although there is strong theoretical support for temperature management in cardiac surgery, there are few actual studies demonstrating its efficacy.Christopher M. Horn ,1 Chung-Huan J. Sun ,1 Raul G. Nogueira ,1 Vishal N. Patel ,1 Arun Krishnan ,2 Brenda A. Glenn ,1 Samir R. Belagaje ,1 Tommy T. Thomas ,1 Aaron M. Anderson ,1 Michael R. Frankel ,1 Kiva M. Schindler ,1 Rishi Gupta 11Department of Neurology, Emory University School of Medicine, Marcus Stroke and Neuroscience Center, Grady Memorial Hospital, Atlanta, Georgia.2Department of Radiology, Emory University School of Medicine, Atlanta, Georgia.Endovascular Reperfusion and Cooling in CerebralAcute Ischemia (ReCCLAIM I)Efficacy of hypothermia as a neuroprotectant has yet to be demonstrated in acute ischemic strokes. We conducted a phase I pilot study to assess the feasibility and safety of performing intravascular hypothermia after definitive intra-arterial reperfusion therapy (IAT). ReCCLAIM was a prospective single arm open-label clinical trial conducted between May-August 2012 at Grady Memorial Hospital. Twenty patients with ASPECTS 5–7 and NIHSS>13 were enrolled and treated with intravascular cooling immediately after IAT. Incidences of pneumonia, DVT, cardiac arrhythmias, and post-op hemorrhages were documented for the entire length of stay. Secondary outcomes included blood brain barrier (BBB) breakdown on Gad-enhanced MRIs and 90 day modified Rankin scores. The mean age, median NIHSS and median final infarct volume was 59.7±14.6 years, 19 (IQR16–22) and 78 cm3 (IQR16–107) respectively. The average time to target temperature, 33°C, was 64±50 minutes. Intracranial hemorrhages were found in three patients, of which one was symptomatic. Evidence of BBB breakdown was observed on three (21%) out of 14 MRIs. Six patients died due to withdrawal of care, whereas six patients (30%) achieved mRS of 0–2 at 90 days. In a binary logistical regression model comparing ReCCLAIM patients to 68 historical controls at our institution, hypothermia was protective against intracerebral hemorrhages (OR0.09; 95%CI 0.02–0.56; p<0.01). Hypothermia can be safely performed after definitive IAT in patients with large pre-treatment core infarcts. A phase II study randomizing patients to hypothermia or normothermia is needed to properly assess the efficacy of hypothermia as a neuroprotectant for reperfusion injury.Rainer Kollmar Neurology and Neurogeriatrics, Darmstadt Hospital, Darmstadt, Germany.Therapeutic hypothermia in large intracerebral hemorrhage – a new treatment option?Large spontaneous intracerebral hemorrhage (ICH) is a severe acute neurological disease which causes high morbidity, mortality, and disability [1]. Major factors for the prognosis of ICH are initial hematoma volume [2], hematoma enlargement [3], or the presence of intraventricular hemorrhage (IVH) [4]. While hematoma volume is a typical target for surgical interventions and prevention of enlargement by normalizing coagulation and blood pressure, IVH can be treated by extraventricular drainage and/or intraventricular thrombolysis. So far, the role of perihemorrhagic edema (PHE) has not been described sufficiently. However, clinical experience and observational studies indicate that large ICH is associated with enlargement and life threatening PHE expansion (5). Therefore, PHE is a promising therapeutic target after ICH. Experimental data shows that blood and blood breakdown products of the ICH initiate a secondary cascade of blood–brain barrier damage and inflammatory processes in the tissue surrounding the hematoma, thereby leading to the development of perihemorrhagic edema (PHE) [6,7]. While there is ongoing debate on how to influence the PHE, rodent models nicely show that therapeutic hypothermia is able to reduce cerebral edema in the acute phase [8,9]. While there is conflicting data about the relevance of TH on outcome after experimental ICH, reduction of the acute and subacute PHE could help to survive the critical phase of ICH treatment in which patients often die from herniation due to PHE and ICH.Clinical data show that PHE increased up to day 11 after ICH onset [5]. Therefore, we have established a clinical protocol for patients with large ICH at the level of basal ganglia or/and thalamus. Typically, clinicians question the adequate treatment, since both surgical evacuation and best medical treatment show only poor results for mortality and functional outcome [10]. We have chosen patients with a size of above 25 ml, since these patients most likely die under medical therapy. We have reported data from our pilot study in which n=12 patients have been treated by mild hypothermia of 35°C for a period of 10 days by endovascular catheters (11). TH has been initiated within a time window below 12 hours from symptom onset. The standard rewarming rate was 0.5°C per 24 hours. Evolution of PHE has been measured on routine cranial CT scans and functional outcome has been assessed after 3 months and one year. Data have been compared to n=25 patients from a prospectively conducted data based on ICH patients. All hypothermic patients (mean age, 60+/−10 years) survived until day 90, whereas 7 patients died in the control group (mean age, 67+/−7 years). Absolute hematoma size on admission was 58+/−29 mL (hypothermia) compared to 57+/−31 mL (control). In the hypothermia group, edema volume remained stable during 14 days (day 1, 53+/−43 mL; day 14, 57+/−45 mL), whereas edema significantly increased in the control group from 40+/−28 mL (day 1) to 88+/−47 mL (day 14). ICH continuously dissolved in both groups. Pneumonia rate was 100% in the hypothermia group and 76% in controls (P=0.08). No significant side effects of hypothermia were observed. While these data have been promising, we have been eager to assess outcome after one year. After 12 months, 2 patients had died, whereas 6 patients (50%) were able to walk without assistance (mRS 3) [12]. After this initial results, we have considered TH for patients with large ICH as an SOP which (a) needs evaluation in a randomized fashion and (b) which can be used for patients not randomized into such a study. Together with the Innsbruck group, we have initiated a randomized controlled trial on TH in large ICH. This Cooling in INtraCerebral Hemorrhage (CINCH) trial has been designed to determine whether TH reduces perihemorrhagic edema and improves survival rates after large ICH [13]. The CINCH trial is a German-Austrian multicenter, randomized controlled trial and will include 50 patients (age 18–65) with acute large primary ICH defined by location (basal ganglia or thalamus) and size (25 to 64 ml on cranial CT). The patients are be randomly allocated between 6 and 18 hours after clinical ICH-symptom onset to two treatment groups: conservative medical treatment or TH. TH of 35°C is initiated and maintained for 8 days by endovascular catheters and is followed by slow controlled rewarming. The primary outcome measures of the study are total lesion volume on CT (ICH plus perihemorrhagic edema on day 8±0.5 and day 11±0.5 after ICH) and mortality after 30 days. Secondary outcomes of interest include in-hospital mortality, mortality after 90 day, functional deficit as defined by the modified Rankin Scale (mRS) and Barthel Index, serious adverse events (SAEs) associated to hypothermia and fever burden during ICU-treatment. The CINCH trial will produce the best available evidence on the effects of TH after large ICH. So far, n=8 patients are included into the study. Patients who could not be included into the study mostly because of the upper age limit have been treated by a similar SOP. Therefore, we could report data of n=25 patients treated by TH because of ICH [14]. We could reproduce the data of our initial case series and showed that PHE volumes in the hypothermia group remained stable, while PHE continuously increased in the historical control group up to day 10. There was a significant difference from day 3 after symptom onset. Shivering (36%) and pneumonia (96%) were the most frequent complications during TH. Mortality rate was 8.3% in TH versus 16.7% in the control group after 3 months and 28 versus 44% after 1 year. Based on current observations, we consider TH over a prolonged period of 8 to 10 days being a treatment alternative to far best medical therapy and/or surgical interventions. To our surprise, functional outcome has been favorable for a meaningful subset of patients considering the severity of disease and previous data on deleterious outcome.Patrick Lyden Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California.Update on the ICTuS 2/3 Trial: Therapeutic Hypothermia for Acute StrokeTherapeutic hypothermia for acute stroke remains under studied. In the Intravascular Cooling in the Treatment of Stroke (ICTuS) trial, awake stroke patients were cooled using an endovascular cooling catheter and a novel anti-shivering regimen. The ICTuS-L study confirmed safety and feasibility of the combination of endovascular hypothermia and thrombolysis. Time to reach target temperature was related to age (p<0.01), BSA (p<0.01) and meperidine (p<0.05). Shivering was well controlled by the combination of meperidine, buspirone, and surface counter-warming. Further analysis of the 26 patients who underwent endovascular hypothermia showed that the risk of pneumonia was increased by BMI and baseline NIHSS but in multivariable logistic regression analysis only NIHSS was marginally associated with risk of pneumonia, after adjustment for BMI (OR: 1.19, 95% CI: 0.98, 1.43; p=0.0740). We designed a novel Phase 2/3 trial to further test the safety of combined thrombolysis and endovascular hypothermia, and to determine if the combination shows superior outcomes (90 day mRS) compared to thrombolysis alone. The ICTuS 2/3 protocol contains novel features designed to achieve critical milestones. Innovations include scrupulous pneumonia surveillance, intravenous chilled saline immediately after randomization to induce rapid cooling, and a requirement for catheter placement within 2 hours of thrombolysis. Our previous experience suggests that it may not be possible to reproducibly target 33°C versus 35°C; the ‘permissive hypothermia’ approach we developed is based on the observation that finer precision may not be possible in awake patients. To date, 56 patients have been enrolled into the ICTuS 2/3 trial.Christopher J. White John Ochsner Heart & Vascular Institute, Ochsner Clinic Foundation, New Orleans, Louisiana.Use of Hypothermia in Myocardial InfarctionTherapeutic hypothermia (TH) has become well accepted for its neurological benefits in survivors of cardiac arrest, however the evidence for the benefit of TH in heart attacks has been controversial. Early reperfusion in ST elevation myocardial infarction (STEMI) with a door to balloon time of ≤90 minutes has been conclusively demonstrated. There is now evidence showing that for every 10 minutes of delay to reperfusion, there is a 1% mortality reduction. There is also accumulating evidence that early reperfusion not only limits ischemic injury, but it also minimizes reperfusion injury. In animal models, TH has been a very effective tool to minimizing reperfusion injury to the heart. Two randomized trials of heart attack patients used internal cooling (COOL MI and ICE IT) and nuclear scans to determine infarct size were not able to show a benefit. When the data was analyzed only for patients who had achieved target temperature (<35°C) there did appear to be a benefit for the TH group. Most recently, the RAPID MI-ICE pilot trial in 20 heart attack patients used a combination of iced saline and internal cooling to achieve rapid TH prior to reperfusion. Using magnetic resonance imaging, they were able to show a statistically significant benefit for heart muscle salvage in the TH group. The key take away points for myocardial salvage in heart attack patients are that rapid achievement of target temperature (<35°C) should be achieved in as short a time as possible (<90 minutes) in order to provide maximum protection from both ischemia and reperfusion injury.Abbot Laptook Department of Pediatrics, Alpert Medical School of Brown University, Providence, Rhode Island.Therapeutic Hypothermia for Neonatal EncephalopathyTherapeutic hypothermia is widely used to treat newborns with hypoxic-ischemic encephalopathy and is the only treatment with evidence from clinical trials. Hypoxic-ischemic brain injury affects newborns via two sequences; acute sentinel events (e.g. placental abruption) or increased vulnerability to the stresses of labor due to maternal, placental or fetal characteristics. Newborn hypoxic-ischemic injury severe enough to result in brain injury always manifests encephalopathy in the neonatal period and brain energy failure. Recovery from initial/primary brain energy failure is followed by a therapeutic window during which initiation of hypothermia can prevent or attenuate injury before a second phase of energy failure triggers injury. There have been 6 large randomized trials demonstrating a benefit of hypothermia for newborns with hypoxic-ischemic encephalopathy. Hypothermia regimes involved reductions of core temperature by ≈3.5°C with whole body cooling or ≈2.5°C with a combination of head and body cooling and were initiated prior to 6 hours of age and continued for 72 hours. Using meta-analysis there is a 24% reduction in death or disability at 18 months of age with no serious adverse effects. However, 40–45% of infants have a poor outcome even with therapy. Follow-up of infants in one trial to 6–7 years indicates a reduction in death without an increase in neurologically impaired infants. Current investigation includes effective dissemination of the therapy and strategies to improve outcomes for treated infants. Therapeutic hypothermia is provided by tertiary/quaternary centers that serve regional areas; 50% of affected infants are transferred following birth. Devices to cool on transport are limited and uncontrolled cooling is frequent. Clinical trials are addressing refinement of hypothermia regimens or combining hypothermia with other neuroprotective treatments.Markus Foedisch , A. Viehoefer , C. Buschmann Department of Anesthesia and Intensive Care Medicine, Evangelische Kliniken, Bonn, Germany.Brain Damage Markers (NSE, S100B) And Determination Of Prolonged Hypothermia After Cardiac Arrest – Data From The Coolbrain Registry BonnResuscitative therapeutic hypothermia (RTH) after cardiopulmonary resuscitation (CPR) is recommended for improvement of neurological outcome in comatose survivors of cardiac arrest (CA). According to experiences from the HACA trial most post-CA centers maintain RTH for 24 hours at 33°C core temperature (Europe: 93%). Nevertheless no randomized clinical studies exist showing an optimal duration of cooling after CA and only few case reports underlie a possible need for a longer duration of cooling in special cases of CA. Data from animal studies show, that the duration of hypothermia required to protect the brain is dependent on the severity and duration of ischemia. This underlies the possible importance of extended hypothermia treatment in cases of prolonged hypoxemia, long durance of CPR and CA due to non-coronary causes. It has to be asked if and how patients can be selected early in the course of therapy with the need of prolonged RTH. Even if they have relatively poor sensitivity, certain brain damage markers (NSE, S100B) do have prognostic potential and can serve as a means to guide therapy. The time course of NSE concentrations during the first three days after ROSC can be relevant for outcome prognosis and significantly differs between patients with good and bad neurological outcome. Based on these findings a subgroup of patients suffering from severe brain injury due to the origin of CA (non-cardiac/asphyxial causes, prolonged CPR and/or severe low cardiac output syndrome) and initial NSE/S100B concentrations underlying substantial neurological damage were treated with RTH for 72 hours using a standardized post-cardiac arrest and cooling protocol. Mean NSE values were 43,3 μg/ml one hour after ROSC; mean S100B values were measured 1,95 μg/l respectively. The majority of the patients (65%) showed good neurological outcome with a CPC 1/2 on ICU discharge, 10% had a CPC 3 and 5% a CPC 5 at the same endpoint. No differences in adverse events or hypothermia related complications could be documented. All patients with a good neurological outcome showed a significant decrease of NSE levels between 48 and 72 hours after ROSC, whereas the group with bad neurological outcome (CPC>3) had a constant elevation or increase of NSE concentrations during the same time frame. S100B levels decreased into normal range between 24 and 48 hours independent of outcome. These findings influenced the post-cardiac arrest and cooling protocols for patients with hypoxic origin of CA and all patients with initial high and constant increased levels of brain damage markers leading to a targeted temperature management including aggressive normothermia after the rewarming process for more than 144 hours. Obtaining daily levels of brain damage markers obviously provide additional and valuable information about the patient's course during post-cardiac arrest treatment and therefore can improve the diagnostic and therapeutic approach leading towards extended duration of RTH. The NSE course showed superior performance to S100B as guide for prolonged cooling. For defining optimal duration of RTH after CA and determination of patients to be selected for this therapeutic approach more randomized studies should be initiated.Michael Le May Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.Code ROSC, Survival, and Length of Hospitalization in Patients Treated With Therapeutic HypothermiaSurvival is improved in patients successfully resuscitated from out of hospital cardiac arrest (OHCA) with the use of therapeutic hypothermia (TH). We review survival resulting from a regional program initiated at our cardiac center for patients with return of spontaneous circulation (ROSC) who remain comatose after resuscitation. We identified patients presenting with OHCA managed with TH from the University of Ottawa Heart Institute Code ROSC database. Cooling was done with pads or an endovascular device. We report on univariate predictors for hospital survival and factors associated with length of stay.Between Aug 2010 and Sept 2012, 104 consecutive patients were treated with TH: the mean age was 61±14 yr, 75% were male, 25% had diabetes mellitus, 25% prior MI and 47% STEMI. Cardiac arrest was witnessed in 72% and VFib/pulseless VT was the presenting rhythm in 84%. Coronary angiography was performed in 89% and PCI in 64%. Survival was recorded in 62.5%. Survival was associated with: lower age, 58±13 vs. 65±13, p=0.007; shorter downtime, 19±11 vs. 21±23 min, p=0.04, VFib/VT as presenting rhythm, in 74% vs. 13%, p=0.001; absence of shock, in 71% vs. 47%, p=0.03; and endovascular cooling, in 33.8% vs. 15.4%, p=0.04. The mean length of hospitalization for patients with STEMI was 12±18 vs. 21±11 days for patients without STEMI, p=0.004; 8±14 for non survivors, vs. 23±14 for survivors. A Code ROSC regional program is feasible and appears to be associated with survival benefits in patients with OHCA. However the mean length of hospitalization for these patients remains high.Justin Lundbye Hospital of Central Connecticut, Hartford Hospital and the University of Connecticut, New Britain, Connecticut.Therapeutic Hypothermia. Beyond Standard PracticeSince 2006, survival from out of hospital cardiac arrest has substantially improved. This is believed to be in part due to the institution of therapeutic hypothermia across the United States. Patients are being cooled for both non-shockable as well as shockable rhythms with randomized trials supporting the latter. However, in-hospital cardiac arrest patients still are not consistently cooled. Additionally, patients with ST segment elevation myocardial infarction should also receive therapeutic hypothermia after a cardiac arrest. It does not seem to impact door to balloon time but may indeed improve outcome. There are several modalities available to induce therapeutic hypothermia including surface as wel