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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-six infants with hypoxic-ischemic encephalopathy (HIE) were randomized to normothermia or to systemic hypothermia. The hypothermia group had less cortical gray matter signal abnormality on magnetic resonance imaging (MRI) (1/12 vs 7/14 infants in the normothermic group; P = .036), which may indicate differing regional benefit from systemic hypothermia.
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PMID:Randomized trial of systemic hypothermia selectively protects the cortex on MRI in term hypoxic-ischemic encephalopathy. 1558 Jan 90

Hypoxic-ischemic injury may cause multisystem organ damage with significant aberrations in clotting, renal, and cardiac functions. Systemic hypothermia may aggravate these medical conditions, such as bradycardia and increased clotting times, and very little safety data in neonatal hypoxic-ischemic injury is available. This study reports a multicenter, randomized, controlled pilot trial of moderate systemic hypothermia (33 degrees C) vs normothermia (37 degrees C) for 48 hours in infants with neonatal encephalopathy instituted within 6 hours of birth or hypoxic-ischemic event. The best outcome measures of safety were determined, comparing rates of adverse events between normothermia and hypothermia groups. A total of 32 hypothermia and 33 normothermia neonates were enrolled in seven centers. Adverse events and serious adverse effects were collected by the study team during the hospital admission, monitored by an independent study monitor, and reported to Institutional Review Boards and the Data and Safety Monitoring Committee. The following adverse events were observed significantly more commonly in the hypothermia group: more frequent bradycardia and lower heart rates during the period of hypothermia, longer dependence on pressors, higher prothrombin times, and lower platelet counts with more patients requiring plasma and platelet transfusions. Seizures as an adverse event were more common in the hypothermia group. These observed side effects of 48 hours of moderate systemic hypothermia were of mild to moderate severity and manageable with minor interventions.
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PMID:Moderate hypothermia in neonatal encephalopathy: safety outcomes. 1645 38

A period of secondary energy failure consisting of a decline in phosphocreatine/inorganic phosphate (PCr/Pi), a rise in brain lactate, and alkaline intracellular pH (pH(i)) has been described in infants with neonatal encephalopathy. Strategies that ameliorate this energy failure may be neuroprotective. We hypothesized that a neonatal rat brain slice model undergoes a progressive decline in energetics, which can be ameliorated with hypothermia or amiloride. Interleaved phosphorus ((31)P) and proton ((1)H) magnetic resonance (MR) spectra were obtained from 350 microm neonatal rat brain slices over 8 h in a bicarbonate buffer at 37 degrees C and at 32 degrees C in 7- and 14-d models. (31)P MR spectra were obtained with amiloride in a bicarbonate-free buffer at 37 degrees C in the 14-d model. Findings were similar in 7- and 14-d models. In the 14-d model, there was a Pi doublet structure corresponding to alkaline pH(i) values of 7.50 +/- 0.02 and 7.21 +/- 0.04. Compared with the stabilized baseline of 100, at 5 h PCr/Pi was 65 +/- 6.3 and lactate/NAA was 187 +/- 3 at 37 degrees C, but PCr/Pi and lactate/NAA were not significantly different from baseline at 32 degrees C. Nucleotide triphosphate (NTP)/phosphomonoester (PME) was 0.93 +/- 0.23 at 37 degrees C and 1.81 +/- 0.21 at 32 degrees C at 5 h. With amiloride exposure in the 14-d model, baseline pH(i) values were 7.25 +/- 0.09 and 6.98 +/- 0.02 and NTP/PME was 1.81 +/- 0.05; these parameters were not significantly different at 5 h. Our interpretation of these findings is that the brain slice model underwent secondary energy failure, which was delayed with hypothermia or amiloride.
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PMID:Hypothermia and amiloride preserve energetics in a neonatal brain slice model. 1600 23

An 11-year-old male was admitted to our hospital because of high-grade fever, repetitive seizures, and prolonged impairment of consciousness (Glasgow coma scale E1, M5, V1). His seizures were repetitive complex partial seizures that expanded from the unilateral face to the corresponding side of the body. He sometimes developed secondary generalized seizures. While most seizures lasted 1 or 2 min, intractable seizures also frequently (about 5 times/h) occurred. We diagnosed him as encephalitis/encephalopathy, and treated him with artificial respiration, thiamylal sodium, mild hypothermia therapy, steroid pulse therapy, massive gamma-globulin therapy, etc. Afterwards, he had sequelae, such as post-encephalitic epilepsy (same seizures continued to recur), hyperkinesia, impairment of immediate memory, change in character (he became sunny and obstinate), dysgraphia, and mild atrophy of the hippocampus, amygdala, and cerebrum. However, he could still attend a general junior high school. He was diagnosed as acute encephalitis with refractory, repetitive partial seizures (AERRPS). In this case, he was positive for autoantibody to glutamate receptor Gluepsilon2 IgG or IgM in an examination of blood and spinal fluid, and we presumed that this may have influenced his sequelae. In this case, a combination of mild hypothermia therapy, steroid pulse therapy, and massive gamma-globulin therapy was effective.
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PMID:A case of acute encephalitis with refractory, repetitive partial seizures, presenting autoantibody to glutamate receptor Gluepsilon2. 1619 11

Hypothermia induced by whole-body cooling (WBC) and selective head cooling (SHC) both reduce brain injury after hypoxia-ischemia in newborn animals, but it is not known how these treatments affect the incidence or pattern of brain injury in human newborns. To assess this, 14 term infants with hypoxic-ischemic encephalopathy (HIE) treated with SHC, 20 infants with HIE treated with WBC, and 52 noncooled infants with HIE of similar severity were studied with magnetic resonance imaging in the neonatal period. Infants fulfilling strict criteria for HIE were recruited into the study after assessment of an amplitude-integrated electroencephalography (aEEG). Cooling was commenced within 6 hours of birth and continued for 48 to 72 hours. Hypothermia was not associated with unexpected or unusual lesions, and the prevalence of intracranial hemorrhage was similar in all 3 groups. Both modes of hypothermia were associated with a decrease in basal ganglia and thalamic lesions, which are predictive of abnormal outcome. This decrease was significant in infants with a moderate aEEG finding but not in those with a severe aEEG finding. A decrease in the incidence of severe cortical lesions was seen in the infants treated with SHC.
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PMID:Mild hypothermia and the distribution of cerebral lesions in neonates with hypoxic-ischemic encephalopathy. 1674 Aug 88

The possibility of a therapeutic role for cerebral hypothermia during or after resuscitation from perinatal asphyxia has been a long-standing focus of research. However, early studies had limited and contradictory results. It is now known that severe hypoxia-ischemia may not cause immediate cell death, but may precipitate a complex biochemical cascade leading to the delayed development of neuronal loss. These phases include a latent phase after reperfusion, with initial recovery of cerebral energy metabolism but EEG suppression, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidative metabolism from 6 to 15 h post insult. Although many of the secondary processes can be injurious, they appear to be primarily epiphenomena of the 'execution' phase of cell death. This conceptual framework allows a better understanding of the experimental parameters that determine effective hypothermic neuroprotection, including the timing of initiation of cooling, its duration and the depth of cooling attained. Moderate cerebral hypothermia initiated in the latent phase, between one and as late as 6 h after reperfusion, and continued for a sufficient duration in relation to the severity of the cerebral injury, has been consistently associated with potent, long-lasting neuroprotection in both adult and perinatal species. The results of the first large multicentre randomized trial of head cooling for neonatal encephalopathy and previous phase I and II studies now strongly suggest that prolonged cerebral hypothermia is both generally safe - at least in an intensive care setting - and can improve intact survival up to 18 months of age. Both long-term followup studies and further large studies of whole body cooling are in progress.
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PMID:Therapeutic hypothermia: from lab to NICU. 1620 21

An asphyxiated infant with severe hypoxic-ischemic encephalopathy was treated by brain hypothermia using extracorporeal membrane oxygenation (ECMO). The brain hypothermia using ECMO maintained cardiopulmonary functions and stabilized brain temperatures by stably supply of the cooled blood to the brain. Moreover,we measured the levels of glucose, lactate, ionized calcium and glutamate in plasma. The comparison between these levels in the artery and in the cephalic vein, suggests that glucose, lactate, ionized calcium and glutamate might be used as markers of the effects of hypothermia therapy.
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PMID:Changes of lactate, glucose, ionized calcium and glutamate concentrations in cephalic vein blood during brain hypothermia using extracorporeal membrane oxygenation (ECMO) in a newborn infant with hypoxic-ischemic encephalopathy. 1621 78

The current treatment approach to an infant at risk for progression to neonatal encephalopathy after intrapartum hypoxia-ischemia is threefold: 1) early identification of the infant at highest risk for evolving brain injury based on the criteria of a sentinel event during labor, prolonged depression at birth with the need for resuscitation, and evidence of severe fetal acidemia based on a cord umbilical arterial pH less than 7 and/or a base deficit more than -16 meq per L, with early clinical and/or electroencephalogram assessment of moderate to severe encephalopathy; 2) supportive therapy instituted to maintain adequate ventilation and in particular pCO2 levels in a normal range, mean arterial blood pressure within a normal range so as to avoid perturbations in cerebral perfusion, glucose in a normal range to avoid hypoglycemia, and the judicious treatment of seizures; and 3) neuroprotection--induced hypothermia is currently the only strategy that has been rigorously evaluated in two large, multicenter randomized studies. The first study used selective cooling with a cool cap to a rectal temperature at 34.5 degrees C, and the second study used total body cooling to an esophageal temperature of 33.5 degrees C, with the temperature in both studies maintained for 72 hours. No significant side effects were noted with this degree of cooling. The combined data indicate that hypothermia is associated with a reduction in the incidence of death and/or severe disability at 18 months follow-up, with the most significant effect observed in infants who at the initiation of therapy present with modest encephalopathy and/or do not exhibit electrographic seizures.
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PMID:Induced hypothermia: a novel neuroprotective treatment of neonatal encephalopathy after intrapartum hypoxia-ischemia. 1622 68

Encephalopathy, brain edema and intracranial hypertension are neurological complications responsible for substantial morbidity/mortality in patients with acute liver failure (ALF), where, aside from liver transplantation, there is currently a paucity of effective therapies. Mirroring its cerebro-protective effects in other clinical conditions, the induction of mild hypothermia may provide a potential therapeutic approach to the management of ALF. A solid mechanistic rationale for the use of mild hypothermia is provided by clinical and experimental studies showing its beneficial effects in relation to many of the key factors that determine the development of brain edema and intracranial hypertension in ALF, namely the delivery of ammonia to the brain, the disturbances of brain organic osmolytes and brain extracellular amino acids, cerebro-vascular haemodynamics, brain glucose metabolism, inflammation, subclinical seizure activity and alterations of gene expression. Initial uncontrolled clinical studies of mild hypothermia in patients with ALF suggest that it is an effective, feasible and safe approach. Randomized controlled clinical trials are now needed to adequately assess its efficacy, safety, clinical impact on global outcomes and to provide the guidelines for its use in ALF.
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PMID:Keeping cool in acute liver failure: rationale for the use of mild hypothermia. 1624 52

Hypoxic ischemic encephalopathy is a rare condition associated with high neonatal mortality and morbidity. Two randomized clinical trials have recently been published showing potentially promising results with hypothermia for neonatal encephalopathy. Additional clinical trials are underway to test cooling as a therapeutic modality for hypoxic ischemic encephalopathy. Outcome information about infants treated with hypothermia is available for children up to approximately 2 years of age. Longer-term outcome (ie, school age information) is currently lacking with respect to benefit and risk. Therapeutic hypothermia offers a potentially promising therapy for hypoxic ischemic encephalopathy. Hypothermia for encephalopathy should be considered an evolving therapy because of lack of long-term safety and efficacy data.
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PMID:Hypoxic ischemic encephalopathy and hypothermia: a critical look. 1664 28


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