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

The possibility that hypothermia during or after resuscitation from asphyxia at birth, or cardiac arrest in adults, might reduce evolving damage has tantalized clinicians for a very long time. It is now known that severe hypoxia-ischemia may not necessarily cause immediate cell death, but can precipitate a complex biochemical cascade leading to the delayed neuronal loss. Clinically and experimentally, the key phases of injury 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 starting 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. Studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration in relation to the severity of the cerebral injury, has been associated with potent, long-lasting neuroprotection in both adult and perinatal species. Two large controlled trials, one of head cooling with mild hypothermia, and one of moderate whole body cooling have demonstrated that post resuscitation cooling is generally safe in intensive care, and reduces death or disability at 18 months of age after neonatal encephalopathy. These studies, however, show that only a subset of babies seemed to benefit. The challenge for the future is to find ways of improving the effectiveness of treatment.
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PMID:Hypothermic neuroprotection. 1655 54

Molecular biological approaches continue to lead to the identification of alterations in expression of genes coding for key central nervous system proteins involved in water homeostasis, energy metabolism and neurotransmitter regulation in acute liver failure (ALF). However, studies aimed at elucidating the pathophysiological consequences of these changes in gene expression are impeded by the lack of a suitable mouse model of ALF. A previous report described hepatic pathology characteristic of ALF resulting from the administration of azoxymethane (AOM) in mice [Matkowskyj, K.A., Marrero, J.A., Carroll, R.E., Danilkovich, A.V., Green, R.M., Benya, R.V., 1999. Azoxymethane-induced fulminant hepatic failure in C57BL/6J mice: characterization of a new animal model. Am. J. Physiol. 277, G455-G462]. In a series of experiments to further assess this treatment as an effective model of ALF, the effects of administration of AOM to male C57BL mice on hepatic and cerebral function were studied. With maintenance of body temperature at 37 degrees C and control of hypoglycemia, mice developed signs of encephalopathy (decreased locomotor activity followed by loss of righting and corneal reflexes) within 16 h of AOM treatment. AOM-treated mice were hyperammonemic, developed spontaneous hypothermia and brain edema. Brain ammonia concentrations were increased to 0.98+/-0.12 mM at coma stages of encephalopathy. Brain amino acid profiles determined by HPLC were typical of ALF in other species including humans. Mild hypothermia (35 degrees C) led to significant attenuation of brain edema, ammonia, and amino acid changes. These findings demonstrate that AOM treatment affords a simple, reproducible mouse model of ALF which may be suitable for the study of the effects of gene manipulation on the cerebral complications of ALF.
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PMID:Neurobiological characterization of an azoxymethane mouse model of acute liver failure. 1656 65

Complications of liver disease are commonly seen in the intensive care unit (ICU). When evaluating patients with liver disease in the ICU, it is important to determine whether it is acute or chronic liver disease. Because the pathophysiological mechanisms differ among acute and chronic liver, they will be consider separately in this review. Significant advances in the management of acute liver failure highlight the importance of intracranial pressure monitoring for Grade III/IV encephalopathy, and suggest that moderate hypothermia may be a promising treatment for these patients with refractory intracranial hypertension. Chronic liver disease is best discussed in terms of the various complications that may ensue such as ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, variceal hemorrhage and hepatic encephalopathy. Each of these conditions will be discussed with specific attention to critical care management.
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PMID:Advances in critical care hepatology. 1667 36

Research on the pathophysiology and treatment of brain damage with special focus on thermal vascular responses is the subject of this minireview. Interruption of cerebral blood supply by vascular obstruction, temporary cardiac arrest or hyperthermia causes a sudden attack of vascular stroke or heatstroke with serious consequences. It may not induce immediate cell death, but can precipitate a complex biochemical cascade leading to a delayed neuronal loss. When testing thermal vasomotor responses by stepwise cooling of isolated carotid arteries, a temperature-proportional dilatation was observed while heating induced the opposite response: a marked vasoconstriction. General hyperthermia with an increased oxygen demand combined with a reduction of blood supply therefore is a serious consequence. At the cellular level an important mechanism involving hyperthermia is the temperature-dependent regulation of K(+) channel tone of vascular smooth muscle. Further, their inhibition through temperature elevation causes vasoconstriction. In heatstroke, which can induce platelet aggregation and the release of the vasoconstrictor serotonin, arterial cooling attenuates this response. General hypothermia is induced to prevent or attenuate neurological damage in stroke. The procedure is not without serious side effects. Therefore, rapid institution of selective brain cooling has been considered in adults and in infants with postpartum encephalopathy.
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PMID:Thermal reactions of blood vessels in vascular stroke and heatstroke. 1676 3

Hypoxic-ischemic cerebral injury that occurs during the perinatal period is one of the most commonly recognized causes of severe, long-term neurologic deficits in children; it is often referred to as cerebral palsy. Despite improvements in perinatal practice during the past several decades, the incidence of cerebral palsy attributed to intrapartum asphyxia has remained essentially unchanged, primarily because management strategies were supportive and not targeted toward the processes of ongoing injury. Two processes of neuronal injury can be demonstrated after hypoxia-ischemia: neuronal necrosis and apoptosis. Because the mechanisms of these processes likely differ, strategies to minimize brain damage in an affected infant after hypoxia-ischemia likely will have to include interventions that target both processes. The goals of management of a newborn infant who has sustained a hypoxic-ischemic insult and is at risk for evolving injury should include (1) early identification of the infant at highest risk for evolving to the syndrome of hypoxic-ischemic encephalopathy, (2) supportive care to facilitate adequate perfusion and nutrients to the brain, and (3) consideration of interventions to ameliorate the processes of ongoing brain injury. Although the neurology group was unable to develop a definitive framework for the study of neuroprotective strategies for neonatal encephalopathy, it (1) listed key questions to be addressed before exploring possible study designs for managing hypoxic-ischemic encephalopathy in neonates, (2) identified important study-design issues, (3) determined general principles and key elements for neuroprotective-treatment strategies, (4) identified potential treatment strategies, (5) proposed a clinical-trial framework, and (6) identified key elements for a potential clinical-trial framework comparing hypothermia with hypothermia "plus" for moderate-to-severe encephalopathy.
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PMID:Summary proceedings from the neurology group on hypoxic-ischemic encephalopathy. 1677 19

Cerebral palsy (CP) is a group of disorders of movement and posture resulting from nonprogressive disturbances of the fetal or neonatal brain. More than 80% of cases of CP in term infants originate in the prenatal period; in premature infants, both prenatal or postnatal causes contribute. The most prevalent pathological lesion seen in CP is periventricular white matter injury (PWMI) resulting from vulnerability of the immature oligodendrocytes (pre-OLs) before 32 wk of gestation. PWMI is responsible for the spastic diplegia form of CP and a spectrum of cognitive and behavioral disorders. Oxidative stress and excitotoxicity resulting from excessive stimulation of ionotropic glutamate receptors on preOLs are the most prominent molecular mechanisms for PWMI. Asphyxia around the time of birth in term infants accounts for less than 15% of CP in developed countries but the incidence is higher in underdeveloped areas. Asphyxia causes a different pattern of brain injury and CP than is seen after preterm injuries. This type of CP is associated with the clinical syndrome of hypoxic-ischemic encephalopathy shortly after the insult, and the cortex, basal ganglia, and brainstem are selectively vulnerable to injury. Experimental models indicate that neurons in the neonatal brain are more likely to die by delayed apoptosis extending over days to weeks than those in the adult brain. Neurons die by glutamate-mediated excitotoxicity involving downstream caspase-dependent and caspase-independent cell death pathways. Recent reports indicate that males and females preferentially utilize different pathways. Clinical trials indicate that mild hypothermia reduces death or disability in term infants following asphyxia and basic research suggests that this approach might be combined with pharmacological strategies in the future.
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PMID:Cerebral palsy. 1702 68

Worldwide, viral hepatitis is the leading cause of acute liver failure, whereas acetaminophen hepatotoxicity is the most commonly identified cause in Western countries. Restricting the quantity of acetaminophen tablets dispensed has been shown to reduce morbidity and mortality in countries with a high incidence of acetaminophen overdose. Troglitazone and bromfenac are two recently approved medications that were withdrawn from the market due to an unacceptably high incidence of severe hepatotoxicity. In addition, trovafloxacin, nefazodone, and ritonavir were reported to be associated with severe hepatitis and acute liver failure. Moderate hypothermia is a simple and potentially effective means of reducing intracranial pressure in patients with acute liver failure and cerebral edema. However, controlled clinical trials are needed to determine proper patient selection and optimize treatment. Extracorporeal bioartificial liver support devices remain an exciting but as yet unproven means of supporting acute liver failure patients with advanced encephalopathy. Living donor liver transplantation has recently been reported for adults and children with acute liver failure. However, ethical concerns regarding donor safety and the ability to obtain informed consent without coercion have been raised. Lastly, advances in the identification and isolation of pluripotent liver stem cells in human bone marrow provides hope for a simple and effective means of enhancing native liver regeneration.
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PMID:Acute liver failure. 1703 Nov 71

A 1-year-old girl with influenza-associated encephalopathy initially exhibited prolonged febrile convulsions and subsequent drowsiness. She became unconsciousness and experienced a cluster of seizures 4 days later. Diffusion-weighted magnetic resonance imaging (DWI) showed high signal intensity in the bilateral frontal white matter. This signal change migrated to the bifrontal cortical areas and the caudate nuclei within 10 days, when T2 elongation appeared over the gray and white matter of frontal lobes. Choreoathetosis and oculogyric crisis were transiently noted at this period. Frontal lobe signs, including the forded mouth opening response, after diminution of these movement disorders. The DWI signal change subsequently resolved and frontal cortical atrophy appeared thereafter. Levels of inflammatory cytokines in the cerebrospinal fluid were normal during the acute phase of clinical course. The biphasic clinical course with initial prolonged seizure, involvement of the frontal lobes, and the progression of signal change on DWI from white to gray matter, meets the characteristics of "status epilepticus-type acute encephalopathy" suggested by Shiomi et al. Although pentobarbital infusion, steroid pulse therapy and mild hypothermia did not show any apparent effects on the clinical course of this patient, further trial of these therapies may be warranted for the treatment of this type of encephalopathy.
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PMID:[Influenza-associated encephalopathy with onset of prolonged convulsion: a case report]. 1709 68

There is growing acceptance within the medical community of induced (therapeutic) hypothermia as a tool to achieve neuroprotection and/or cardioprotection. Although much work remains to be done in identifying those clinical situations in which hypothermia can be effective, there is now sufficient evidence to regard it as a standard of care, at least for some indications such as selected patients with postanoxic encephalopathy. Thus, attention is now partly shifting from assessment of the clinical evidence of efficacy to technical and implementation issues. This review provides a list of criteria by which cooling devices can be judged, and specifically it discusses one of the new cooling devices: the Alsius CoolGard 3000 device and CoolLine catheter. General aspects and advantages/disadvantages of surface versus core cooling are discussed, as are potential side effects, device-specific pros and cons, and cost-effectiveness issues. In addition, the current state of the evidence for use of induced hypothermia for various indications is briefly reviewed.
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PMID:Equipment review: cooling catheters to induce therapeutic hypothermia? 1709 65

Evidence suggests that hypothermia for hypoxic ischemic encephalopathy in the term neonate may decrease the risk of death or neurodevelopmental impairment. The objective of this study was to determine how hypothermia has been incorporated into practice. An anonymous survey was sent to medical directors of United States neonatal intensive care units (NICUs) in October 2005. We received completed surveys from 441 (54.5%) of 809 of NICUs. Only 6.4% of respondents used hypothermia. The most common method was total body cooling (64.3%) compared with head cooling (25%) or both (10.7%). At centers that did not offer hypothermia, 29% transferred infants to an institution that did. Centers that offered hypothermia were more likely at academic institutions (76.9%) compared with private practices (11.5%; p < 0.001). Hypothermia was more likely offered at institutions that offered extracorporeal membrane oxygenation (ECMO; 57%) than centers where ECMO was not offered (43%; p < 0.001). There has not been widespread use of hypothermia. There are a variety of protocols used. As results of further outcome studies become available, educational efforts and national practice guidelines will be essential.
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PMID:Hypothermia for the treatment of neonatal ischemic encephalopathy: is the genie out of the bottle? 1719 47


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