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

Heatstroke is a life-threatening illness characterized by an elevated core body temperature (>40 degrees C) and dysfunction of central nervous system, which results in delirium, convulsions, or coma. Despite adequate hypothermia or other care-therapy, heatstroke is often fatal. On the basis of our knowledge of the pathophysiology on heatstroke, we hypothesized that heatstroke is a form of hyperthermia associated with the acute physiological alterations, the cytotoxicity of heat, systemic inflammatory response, oxidative damage and attenuated heat-shock response leading to a syndrome of multi-organ dysfunction. In view of above-mentioned situation, the physiological factors underlying heatstroke and the corresponding possible therapeutic strategies to avert the complications of this disorder would be summarized in this review so as to provide some therapeutic guidelines for heatstroke. Heatstroke is a very complicated process. Acute physiological alterations, such as low arterial hypotension, intracranial hypertension, cerebral hypoperfusion, cerebral ischemia, and increased intracellular metabolism rate, occurred while exposed to a high ambient temperature. Hyperpyrexia caused cytotoxicity, resulting the degradation and aggregation of extensive intracellular proteins, influencing the change of membrane stability and fluidity, damaging the transmembrane transport of protein and the function of surface receptor, and inducing different cytoskeletal changes. Heatstroke resembles sepsis in many aspects, and endotoxemia and cytokines may be implicated in its pathogenesis. The concentration of interleukin-6 was positively correlated with the severity of heatstroke. The excessive accumulation of cytotoxic free radicals and oxidative damage may occur in the brain tissues during the genesis and development of heatstroke. The circulatory shock and cerebral ischemia resultant from heatstroke correlated closely with the free radicals (especially free radicals of peroxide and superoxide), the peroxidation of lipids, and low activity of antioxidase in the brain. Heat-shock proteins (Hsps) played a critical role during the process obtaining thermotolerance, therefore, protected from stress-induce cellular damage. Host factors or physiologically limiting factors, for instance, aging, existing illness, dehydration, deep insomnia, lack of acclimation to heat, inadequate physical fitness, and certain genetic polymorphisms were associated with a low level of Hsps expression and might favor the progression from heat stress to heatstroke. Some measures, such as molecular chaperonines, anti-inflammatory agents, antioxidant agents, and modulators of Hsps would be good for the patients with heatstroke.
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PMID:Pathophysiological factors underlying heatstroke. 1663 16

Hyponatremia is often associated with arginine vasopressin (AVP) dysregulation that is regulated by the hypothalamo-neurohypophyseal tract in response to changes in plasma osmolality, commonly in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Potentially lethal complications of hyponatremia most frequently involve the central nervous system and include anorexia, fatigue, lethargy, delirium, seizures, hypothermia and coma, and require prompt treatment. Chronic hyponatremia also complicates patient care and is associated with increased morbidity and mortality, particularly among patients with congestive heart failure. Conventional treatments for hyponatremia (e.g. fluid restriction, diuretic treatment, and sodium replacement) may not be effective in all patients and can lead to significant adverse events. Preclinical and clinical trial results have shown that AVP receptor antagonism is a promising approach to the treatment of hyponatremia that directly addresses the effects of increased AVP and consequent decreased aquaresis, the electrolyte-sparing excretion of free water. Agents that antagonize V(2) receptors promote aquaresis and can lead to increased serum sodium. Dual-receptor antagonism, in which both V(2) and V(1A) receptors are blocked, may provide additional benefits in patients with hyponatremia.
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PMID:Hyponatremia, arginine vasopressin dysregulation, and vasopressin receptor antagonism. 1717 May 24

Postoperative cognitive dysfunction, confusion, and delirium are common after general anesthesia in the elderly, with symptoms persisting for months or years in some patients. Even middle-aged patients are likely to have postoperative cognitive dysfunction for months after surgery, and Alzheimer's disease (AD) patients appear to be particularly at risk of deterioration after anesthesia. Several investigators have thus examined whether general anesthesia is associated with AD, with some studies suggesting that exposure to anesthetics may increase the risk of AD. However, little is known on the biochemical consequences of anesthesia on pathogenic pathways in vivo. Here, we investigated the effect of anesthesia on tau phosphorylation and amyloid precursor protein (APP) metabolism in mouse brain. We found that, regardless of the anesthetic used, anesthesia induced rapid and massive hyperphosphorylation of tau, rapid and prolonged hypothermia, inhibition of Ser/Thr PP2A (protein phosphatase 2A), but no changes in APP metabolism or Abeta (beta-amyloid peptide) accumulation. Reestablishing normothermia during anesthesia completely rescued tau phosphorylation to normal levels. Our results indicate that changes in tau phosphorylation were not a result of anesthesia per se, but a consequence of anesthesia-induced hypothermia, which led to inhibition of phosphatase activity and subsequent hyperphosphorylation of tau. These findings call for careful monitoring of core temperature during anesthesia in laboratory animals to avoid artifactual elevation of protein phosphorylation. Furthermore, a thorough examination of the effect of anesthesia-induced hypothermia on the risk and progression of AD is warranted.
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PMID:Anesthesia leads to tau hyperphosphorylation through inhibition of phosphatase activity by hypothermia. 1737 70

A total of 106 patients aged 60,2+/-8,7 years were entered in the study. They underwent surgery on the open heart (coronary artery bypass grafting) using cardiopulmonary bypass (78 patients) under normothermic (38 patients) or hyporthermic (36 patients) conditions. The control group consisted of patients who underwent surgery on the working heart without the use of cardiopulmonary bypass (32 patients). Patients were studied before the operation and on the 5th and 14th days after it. In the preoperative period, psychic pathology was detected in more than half of patients. Neurotic disorders prevailed and affective disorders and the psychoorganic syndrome were detected as well. In the early postoperative period, an increase of frequency of mental disorders was noted in all groups, the clinical picture being more complicated. Memory and intellectual insufficiency of transitory nature measured with the Mini Mental State Examination (MMSE) scale was revealed. Cases of postcardiotomic delirium were observed. Patients of the normothermic group demonstrated milder signs and faster reduction of part of mental disorders as compared to the hypothermic group. The results of the study suggest that the normothermic method versus hypothermia is more preferential for the postoperative psychic state of cardiac patients.
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PMID:[Structure and dynamics of mental disorders in patients before heart surgery and in the early postoperative period.]. 1847 75

Aging is a consequence of progressive decline in special and somatosensory functions and specific brain stem nuclei. Many senescent stigmata, including hypoxia, hypoxemia, depressed cerebral blood flow and glucose metabolism, diseases of senescence, and their medications all enhance hypothermia as do alcohol, cold environment, and malnutrition. Hypothermia is a critical factor having deleterious impact on brain stem and neocortical functions. Additionally, anesthesia in elderly also promotes hypothermia; anesthetics not only cause consciousness (sensory and motor) changes, but memory impairment as well. Anesthesia inhibits cholinergic pathways, reticular and thalamocortical systems, cortico-cortical connectivity, and causes post-operative delirium and cognitive dysfunction. Increasing evidence indicates that anesthetic exposures may contribute to dementia onset and Alzheimer's disease (AD) in hypothermic elderly. Inhaled anesthetics potentiate caspases, BACE, tau hyperphosphorylation, and apoptosis. This paper addresses the important question: "Why do only some elderly fall victim to AD"? Based on information on the pathogenesis of early stages of cognitive dysfunction in elderly (i.e., due to senescent stigmata), and the effects of anesthesia superimposed, a detailed plausible neuropathological substrate (mechanism/pathway) is delineated here that reveals the possible cause(s) of AD. Basically, it encompasses several risk factors for cognitive dysfunction during senescence plus several hypothermia-enhancing routes; they all converge and tip the balance towards dementia onset. This knowledge of the confluence of heterogeneous risk factors in perpetuating dementia relentlessly is of importance in order to: (a) avoid their convergence; (b) take measures to stop/reverse cognitive dysfunction; and (c) to develop therapeutic strategies to enhance cognitive function and attenuate AD.
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PMID:Conversion of elderly to Alzheimer's dementia: role of confluence of hypothermia and senescent stigmata--the plausible pathway. 2150 31

The innovative concept of transnasal evaporative cooling for therapeutic hypothermia in cardio-pulmonary-cerebro-resuscitation has therapeutic implications with evidence of rapid and selective brain cooling; however, this author wants to elicit that this concept may hold answers for many physiological phenomena which have not been explored or completely understood up till now. To affirm the physiological role of transnasal cooling, the innovative non-invasive brain temperature monitoring can help the investigators to explore and understand the following transnasal pathophysiological phenomena: (1) understanding correlation of brain temperature and sinus headache secondary to nasal blockade, (2) exploring the therapeutic role of nasal oxygen for prevention of delirium in intubated patients, (3) realizing the impact of controlled enclosed environments on the mood and affect of the inhabitants, (4) understanding the etio-pathogenesis of claustrophobia after excluding the confounding factors of morbid obesity, severe cardiopulmonary disease and incapacitating musculoskeletal diseases, (5) exploring the anthropological role of male pattern of moustache, beard and hair loss, and (6) possible development of a coolant moustache as proposed by the author. In summary, transnasal pathophysiology offers many promising lines of fruitful research to explore the non-olfactory physiological functions of nose in human beings.
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PMID:Transnasal cooling: a Pandora's box of transnasal patho-physiology. 2160 Jun 99

Contributions from the neurosciences to Critical Care in 2011 covered an array of topics. We learned about potential biomarkers for, and the effect of cerebral oxygen metabolism on, delirium, in addition to treatment of the latter. A group of investigators studied surface cooling in healthy awake volunteers, and incidence of infection associated with therapeutic hypothermia. The effects of statin and erythropoietin on stroke were revisited, and the role of adhesion molecule in the inflammatory reaction accompanying intracerebral hemorrhage was scrutinized. Biomarkers in subarachnoid hemorrhage and their relationship to vasospasm and outcome, and effect of daylight on outcome in this patient population, as well as a new meta-analysis of statin therapy were among the research in subarachnoid hemorrhage. Moreover, 2011 witnessed the publication of a multidisciplinary consensus conference's recommendations on the critical care management of subarachnoid hemorrhage. Results of studies regarding the diagnosis and vascular complications of meningitis were reported. Traumatic brain injury received its share of articles addressing therapy with hypertonic saline and surgical decompression, the development of coagulopathy, and biomarkers to help with prognostication. Finally, research on the treatment of Guillain-Barre syndrome in children, prediction of long-term need of ventilatory support, and pathophysiology of critical illness polyneuropathy and myopathy were reported.
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PMID:Year in review 2011: Critical Care--Neurocritical care. 2325 71

A 34-year-old man with uncontrolled hypertension suffered a ventricular fibrillation cardiac arrest from an obstructive left anterior descending artery occlusion. He was defibrillated more than 10 times before achieving return of spontaneous circulation. He was comatose after his arrest and was treated with therapeutic hypothermia, and a bare metal stent was placed in his obstructed coronary artery with restoration of excellent postobstruction blood flow. His postarrest course was complicated by cardiogenic shock; prolonged ventilator-dependent respiratory failure requiring tracheostomy; tracheobronchitis, with cultures positive for methicillin-resistant Staphylococcus aureus (MRSA); and an extended period of agitation and delirium. Thirty-four days after his arrest, his mental status started to improve rapidly. His delirium resolved, he became oriented and lucid, and he was able to be discharged to a rehabilitation facility on hospital day 41, with an excellent prognosis and close follow-up in primary care, cardiology, tracheostomy, and coumadin clinics. He returned to the emergency department 65 days later with the complaint of intermittent chest pain of 4 days' duration. Upon physical examination he was found to have Beau's lines on his fingernails. He was admitted to the hospital for a rule-out myocardial infarction workup, which was uneventful. He was discharged to home in good condition 2 days later.
Ther Hypothermia Temp Manag 2013 Dec
PMID:Beau's Lines After Cardiac Arrest. 2483 50

The evidence is quite clear that ITH in the prehospital setting is of dubious benefit. But what is the harm in continuing the practice? Well, prehospital ITH most likely takes away from more beneficial therapies such as high-quality CPR, rapid defibrillation, recognition of ST-segment elevation myocardial infarction (STEMI), and similar essential treatments. Several studies have shown prehospital ITH, in many cases, delays hospital transport. When the initial studies of ITH were released, I was immediately on the ITH bandwagon. Interestingly, the American Heart Association (AHA) has never recommended prehospital ITH. Even the position paper on ITH by the National Association of EMS Physicians (NAEMSP) was cautious, saying, "A lack of evidence on induced hypothermia in the prehospital setting currently precludes recommending this treatment modality as standard of care for all emergency medical services (EMS) patients resuscitated from cardiac arrest. A systematic review of ITH recently published states, "In cardiac arrest, the initiation of therapeutic hypothermia in the out-of-hospital environment has not been shown to improve neurologic outcomes, although studies to date have been limited. We now know that caution Fxercised by the AHA and preMSP was appropriate. One medmy mentors in residency and ays said, "Never be the first- Univtor to prescribe a new drug or of Mlast doctor to prescribe an old is th" Lik" many things in EMS, EMS tms something that was put in Practe with good intent but lim- scientific evidence. We now P ITH is probably not a good ice and it is time to abandon it. However, we should still carry chilled IV fluids for hyperthermia, excited delirium and to main- tainormothermia in patients in cardiac arrest where transport times are long.
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PMID:Is it time to stop chilling? Induced therapeutic hypothermia doesn't appear to have the prehospital effect we thought it did. 2580 8

Sedation of critically ill patients undergoing mechanical ventilation should be minimized or completely avoided. Only in selected situations is sedation indicated as first line therapy (increased intracranial pressure or therapeutic hypothermia). The critical care physicians primary objective should be to focus on the reversible causes of agitation, such as: pain, anxiety, delirium, dyspnea, withdrawal symptoms, sleep or gastrointestinal symptoms. If sedation is used a validated sedation scale is recommended. On a daily basis sedation should be interrupted and only restarted after a thorough search for reversible causes of discomfort and stress.
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PMID:Danish national sedation strategy. Targeted therapy of discomfort associated with critical illness. Danish Society of Intensive Care Medicine (DSIT) and the Danish Society of Anesthesiology and Intensive Care Medicine (DASAIM). 2587 38


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