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- Risk Factors for Intraventricular Hemorrhage in Term Asphyxiated Newborns Treated With Hypothermia. [JOURNAL ARTICLE]
- Pediatr Neurol 2014 Feb 10.
Intraventricular hemorrhage is rare in term newborns. Severe asphyxia is recognized as one of the risk factors of intraventricular hemorrhage in these newborns. Therapeutic hypothermia, which is the only available treatment for the limitation of brain injury in term asphyxiated newborns, may cause fluctuations of cerebral blood flow, possibly placing the newborn more at risk for intraventricular hemorrhage. The literature regarding the incidence of intraventricular hemorrhage in the context of neonatal hypoxic-ischemic encephalopathy and hypothermia is sparse.We present a clinical observation and review the literature regarding the risk factors for intraventricular hemorrhage in term asphyxiated newborns treated with hypothermia.We describe the clinical course of a term newborn with severe hypoxic-ischemic encephalopathy who developed significant intraventricular hemorrhage during the rewarming period after the 72-hour hypothermia.This newborn presented several risk factors for intraventricular hemorrhage, including severe asphyxia, hemodynamic instability, hemostasis disturbances, instrument delivery, venous sinus thrombosis, and hypoglycemia. Hypothermia and rewarming also may have contributed by causing fluctuations in cerebral blood flow.
- New indicator of postoperative delayed awakening after total aortic arch replacement. [JOURNAL ARTICLE]
- Eur J Cardiothorac Surg 2014 Apr 9.
Impact of the decrease of regional cerebral oxygen saturation (rSO2) on postoperative delayed awakening after total aortic arch replacement (TAR) was validated.From 2008 to 2013, 143 consecutive patients underwent TAR using selective antegrade cerebral perfusion. rSO2 was monitored using near-infrared spectroscopy. We calculated a percent decrease of rSO2 (%-D) immediately after rewarming according to the following formula: %-D = rSO2 (X1) - rSO2 (X2)/rSO2 (X1) × 100 (%), where rSO2 (X1) was measured at the beginning of rewarming, and rSO2 (X2) was measured 10 min later. Delayed awakening was defined as patients not waking up for more than 6 h after the termination of anaesthesia.The average time to wake up was 3.6 ± 2.0 h. Fourteen patients showed delayed awakening. %-D showed a positive linear relationship to awakening time (y = 0.67x - 0.7, r = 0.23, P = 0.007) and receiver operating characteristic analysis showed %-D had a good predictive value for delayed awakening (area under the curve = 0.84). %-D was significantly different between the delayed awakening and the normal group (7.1 ± 5.1 vs 1.3 ± 6.6%, P = 0.002). Two patients (1.4%) who had multicomorbidity with higher %-D died in the hospital due to colon necrosis and sepsis. There were significant differences between patients with normal and delayed awakening in hospital mortality (P = 0.04) and transient neurological deficit (TND, P = 0.007).The maintenance of rSO2 at the early phase of rewarming may be important to avoid delayed awakening or TND after TAR.
- Platelet Dynamics during Natural and Pharmacologically Induced Torpor and Forced Hypothermia. [Journal Article]
- PLoS One 2014; 9(4):e93218.
Hibernation is an energy-conserving behavior in winter characterized by two phases: torpor and arousal. During torpor, markedly reduced metabolic activity results in inactivity and decreased body temperature. Arousal periods intersperse the torpor bouts and feature increased metabolism and euthermic body temperature. Alterations in physiological parameters, such as suppression of hemostasis, are thought to allow hibernators to survive periods of torpor and arousal without organ injury. While the state of torpor is potentially procoagulant, due to low blood flow, increased viscosity, immobility, hypoxia, and low body temperature, organ injury due to thromboembolism is absent. To investigate platelet dynamics during hibernation, we measured platelet count and function during and after natural torpor, pharmacologically induced torpor and forced hypothermia. Splenectomies were performed to unravel potential storage sites of platelets during torpor. Here we show that decreasing body temperature drives thrombocytopenia during torpor in hamster with maintained functionality of circulating platelets. Interestingly, hamster platelets during torpor do not express P-selectin, but expression is induced by treatment with ADP. Platelet count rapidly restores during arousal and rewarming. Platelet dynamics in hibernation are not affected by splenectomy before or during torpor. Reversible thrombocytopenia was also induced by forced hypothermia in both hibernating (hamster) and non-hibernating (rat and mouse) species without changing platelet function. Pharmacological torpor induced by injection of 5'-AMP in mice did not induce thrombocytopenia, possibly because 5'-AMP inhibits platelet function. The rapidness of changes in the numbers of circulating platelets, as well as marginal changes in immature platelet fractions upon arousal, strongly suggest that storage-and-release underlies the reversible thrombocytopenia during natural torpor. Possibly, margination of platelets, dependent on intrinsic platelet functionality, governs clearance of circulating platelets during torpor.
- A novel rat model of cardiopulmonary bypass for deep hypothermic circulatory arrest without blood priming. [Journal Article]
- Chin Med J (Engl) 2014 Apr; 127(7):1317-20.
Large animal cardiopulmonary bypass (CPB) models are expensive, and prevent assessment of neurocognitive function, and difficulties with long-term recovery. The purpose of this study was to establish a novel rat model of cardiopulmonary bypass for deep hypothermic circulatory arrest without blood priming.Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomized to CPB with deep hypothermic circulatory arrest (DHCA) and control groups, with 10 rats each. The experimental protocols, including blood and crystalloid fluid administration, anesthesia, orotracheal intubation, ventilation, cannulation, and heparinization were identical in both groups. After inducing cardiac arrest, the circuit was turned off and rats were left in a DHCA state for 15 minutes. Rats were rewarmed to 34°C to 35°C over a period of 36 to 42 minutes using CPB-assisted rewarming, a heating blanket, and a heating lamp along with administration of 0.1 mEq of sodium bicarbonate and 0.14 mEq of calcium chloride. The remaining priming volume was reinfused and animals were weaned from CPB.All CPB with DHCA processes were successfully achieved. Blood gas analysis and hemodynamic parameters were in the normal range. The vital signs of all rats were stable.Our CPB circuit has several novel features, including a small priming volume, active cooling/rewarming processes, vacuum-assisted venous drainage, peripheral cannulation without thoracotomy or sternotomy, and an accurate means of monitoring peripheral tissue oxygenation.
- Hypothermia Makes Cerebral Resistance Index a Poor Prognostic Tool in Encephalopathic Newborns. [JOURNAL ARTICLE]
- Neonatology 2014 Mar 25; 106(1):17-23.
Background: Severe neonatal encephalopathy (NE) of hypoxic-ischaemic origin may cause death or life-long disability. Acute encephalopathy may also affect cerebrovascular control. Pourcelot's cerebrovascular resistance index (RI) ≤0.55 was predictive of poor outcome in normothermic NE infants. Recent studies have questioned its predictive power during therapeutic hypothermia (HT). Objective: To assess the predictive power of RI during HT and after rewarming. Methods: 45 infants with NE treated with HT for 72 h had their RI calculated during early (median 11 h) and late (median 62 h) cooling and after rewarming (median 89 h). Poor outcome was defined as death or abnormalities on day 10 magnetic resonance imaging shown to predict severe neuromotor disability. Results: RI ≤0.55 during cooling did not differentiate between good and poor outcome (late cooling, p = 0.08), but was powerful after rewarming (p = 0.004). RI ≤0.55 predicted true poor outcome in 43% (95% confidence interval (CI): 12, 80) during late cooling and in 100% (95% CI: 31, 100) after rewarming. RI >0.55 predicted good outcome in 86% (95% CI: 69, 95) during late cooling and in 89% (95% CI: 74, 96) after rewarming. Conclusions: Low RI is not predictive of poor outcome during HT in NE infants, but regains the predictive power seen in normothermic infants after rewarming. © 2014 S. Karger AG, Basel.
- An Investigation of a Hypothermic to Ischemic Ratio in Patients Following Out-of-Hospital Cardiac Arrest Presenting with a Shockable Rhythm. [JOURNAL ARTICLE]
- Ther Hypothermia Temp Manag 2014 Mar 28.
Targeted temperature management (TTM) improves outcome after out-of-hospital cardiac arrest (OHCA). We hypothesized that there may be a significant relationship between the dose of hypothermia, the time to return of spontaneous circulation (ROSC), and survival to discharge. Retrospective pilot investigation on 99 consecutive OHCA patients with initial shockable rhythm, surviving to admission, and undergoing TTM between 2008 and 2011. Dose of hypothermia was defined as the sum of the induction interval (time to target temperature [from ROSC to 33°C]); the controlled hypothermia interval (from reaching 33°C until rewarming); and the rewarming interval (from 33°C to 37°C). Time to ROSC was measured from pulselessness or 911 call time to ROSC. The ratio between the two was termed the hypothermic to ischemic ratio. Purposeful variable selection for logistic regression modeling was used to assess the influence of the hypothermic/ischemic ratio on survival. Odds ratios (OR) were used to examine the effects of predictor variables on survival. Of 99 patients, eight were excluded for deviation from protocol, death during protocol, or missing data. From the univariate models, survivors were more likely to be younger, have a shorter time to ROSC, and have a larger hypothermic/ischemic ratio. Survivors also had a nonsignificant trend toward a longer time to target temperature. In multivariable modeling, the hypothermic/ischemic ratio was the most significant predictor for survival (OR 2.161 [95% confidence interval 1.371, 3.404]). In this pilot study, the hypothermic to ischemic ratio was significantly associated with survival to discharge for patients with an initial shockable rhythm. Further investigation of the relationship between the dose of hypothermia and time to ROSC for postresuscitation TTM is needed.
- Therapeutic Hypothermia for Cardiovascular Collapse and Severe Respiratory Distress After Amniotic Fluid Embolism. [JOURNAL ARTICLE]
- Ther Hypothermia Temp Manag 2014 Mar 5.
Amniotic fluid embolism (AFE) is one of the most catastrophic complications that can occur during pregnancy or in the immediate postpartum period, frequently complicated by profound shock and cardiovascular collapse as well as severe respiratory distress. Therapeutic hypothermia (TH) is now commonly used to improve neurological outcomes after various types of hypoxic injury and is widely used in the treatment of postanoxic injury after cardiac arrest (CA). To our knowledge, no studies have evaluated whether TH could be effectively used in AFE, and its use for this indication has not been described previously. We describe the case of a 32-year-old woman, who developed clinical manifestations of AFE and suffered a CA in the 29th week of her pregnancy. She received prolonged CPR (40 minutes until ROSC) and remained comatose. TH was induced and maintained for a total of 60 hours using an endovascular device, followed by controlled rewarming and maintenance of strict normothermia. The patient survived and was neurologically intact (CPC 1) at 6 months of follow up.
- Surviving Two Hours of Ventricular Fibrillation in Accidental Hypothermia. [JOURNAL ARTICLE]
- Prehosp Emerg Care 2014 Mar 26.
Abstract Background. Cardiac arrest as a consequence of deep accidental hypothermia is associated with high mortality. Standardized prehospital management as well as rewarming with extracorporeal circulation (ECC) are important factors to improve survival. The objective of this case report is to illustrate the importance of effective cardiopulmonary resuscitation (CPR) and ECC in a cardiac arrest following deep accidental hypothermia. Case report. A 42-year-old man was found unresponsive to external stimuli and pulseless at an outdoor temperature of 1°C. CPR was started at the scene by laypersons, and the emergency medical services (EMS) arrived 5 minutes after the emergency call. Resuscitation according to International Liaison Committee on Resuscitation (ILCOR) guidelines was initiated by EMS. The first recorded rhythm was ventricular fibrillation (VF), which persisted, despite repeated defibrillation. The patient showed signs of severe hypothermia and, during ongoing CPR, was transported to hospital where on arrival the patient's rectal temperature was measured at 22°C. Resuscitation measures were continued and warming was started at the emergency room. Due to persistent VF and deep hypothermia, the patient was transferred to a cardiothoracic surgical unit for rewarming with ECC. At commencement of ECC, CPR had been going for approximately 130 minutes and a total of 38 defibrillations had been made. During this time interval the patients was pulseless. At a core temperature of 30°C, one defibrillation restored sinus rhythm and subsequently stable circulation was achieved. The patient received a further 24 hours of hypothermia treatment at 32-34°C. He was discharged to rehabilitation facilities after 3 weeks of hospital care. Three months after the cardiac arrest the patient was fully recovered, was back to work, and had resumed normal activities. Conclusions. We demonstrate a case of cardiac arrest due to deep accidental hypothermia that stresses the importance of effective CPR and early-stage consideration of the use of ECC for safe and effective rewarming.
- Acute Effects of Normobaric Hypoxia on Hand-Temperature Responses During and After Local Cold Stress. [JOURNAL ARTICLE]
- High Alt Med Biol 2014 Mar 25.
Abstract Keramidas, Michail E, Roger Kölegård, Igor B. Mekjavic, and Ola Eiken. Acute effects of normobaric hypoxia on hand-temperature responses during and after local cold stress. High Alt Med Biol 15:000-000, 2014.-The purpose was to investigate acute effects of normobaric hypoxia on hand-temperature responses during and after a cold-water hand immersion test. Fifteen males performed two right-hand immersion tests in 8°C water, during which they were inspiring either room air (Fio2: 0.21; AIR), or a hypoxic gas mixture (Fio2: 0.14; HYPO). The tests were conducted in a counterbalanced order and separated by a 1-hour interval. Throughout the 30-min cold-water immersion (CWI) and the 15-min spontaneous rewarming (RW) phases, finger-skin temperatures were measured continuously with thermocouple probes; infrared thermography was also employed during the RW phase to map all segments of the hand. During the CWI phase, the average skin temperature (Tavg) of the fingers did not differ between the conditions (AIR: 10.2±0.5°C, HYPO: 10.0±0.5°C; p=0.67). However, Tavg was lower in the HYPO than the AIR RW phase (AIR: 24.5±3.4°C; HYPO: 22.0±3.8°C; p=0.002); a response that was alike in all regions of the immersed hand. Accordingly, present findings suggest that acute exposure to normobaric hypoxia does not aggravate the cold-induced drop in hand temperature of normothermic males. Still, hypoxia markedly impairs the rewarming responses of the hand.
- 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.