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

Experimental studies to this point have not identified a selective neonatal pulmonary vasodilator. They have indicated that the neonatal pulmonary circulation is a complex, active vascular bed that has a number of endogenous vasodilatory mechanisms which oppose vasoconstriction under normal circumstances. It seems likely that a better understanding of how those mechanisms become deranged in various disease states will be required before we can substantially improve our drug therapy in pulmonary hypertensive infants. The data we have outlined above indicate that firm recommendations for drugs and their doses cannot be made. Nonetheless, several principles of therapy can be outlined. Because of the marginal benefits, which have resulted from current drug therapy [9, 24, 34, 79, 84, 100, 107], it seems clear that, at the moment, the most prudent initial course in neonates with pulmonary vasospasm should be nonpharmacologic: restoration of normal blood gases, use of high concentrations of inspired oxygen with hyperventilation to pH 7.6 if cyanosis persists [22, 79], avoidance of agitation and hypothermia [22], and correction of any metabolic derangements [92]. Decreased cardiac output should be identified and treated with blood volume expanders and/or cardiotonic agents as necessary. Finally, if physiologic efforts to lower pulmonary vascular resistance fail, drug therapy sometimes is helpful in effecting salvage. Treated infants should be carefully monitored, not only for signs of improved oxygenation, but also for changes in right-to-left ductal shunting and cardiac output. If a given agent does not produce beneficial effects at a range of doses by 60 min, it is unlikely that prolonged therapy will result in late improvement. In such circumstances, a change in drug therapy is probably indicated. Finally, it would seem wise to use multiple agents with extreme cautions, being careful to pair a direct vasodilator (e.g., nitroprusside, tolazoline, or prostacyclin) with a cardiotonic agent (e.g., isoproterenol or dopamine), or simultaneously administered volume expanders as the individual clinical situation dictates. Further animal experimentation will undoubtedly identify new and promising agents and provide an increasing understanding of the cellular physiology of the newborn pulmonary circulation. However, only careful clinical and experimental studies into the cause(s) of the vasoconstriction in newborns will allow the development of a truly rational approach to specific therapy in the human species.
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PMID:Neonatal 'pulmonary vasodilator' drugs. Current status. 642 57

Nicotine produced a distinct reproducible syndrome in the conscious dog when injected intravenously or intracerebroventricularly. Intravenously administered nicotine (40 micrograms/kg/min for 20 minutes) increased cardiac and respiratory rates and produced analgesia, miosis, hypothermia, behavioral restlessness and emesis. When microinjected into the third cerebral ventricle, nicotine (100-200 micrograms) similarly increased cardiac and respiratory rates and pupillary diameter; and produced behavioral restlessness, emesis, erratic analgesia and maintained wakefulness and a desynchronized EEG. Microinjection of nicotine (5-25 micrograms) into the periaqueductal gray failed to alter any of the parameters studied. Intravenous pretreatment with the opioid antagonist naltrexone (2 mg/kg) influenced the action of intravenous nicotine on certain physiological systems. While naltrexone alone produced a significant degree of tachycardia, miosis, and analgesia, it potentiated the tachypnea and antagonized the miotic response evoked by nicotine. Methionine-enkephalin was detected in perfusates obtained from the lateral cerebral ventricles of conscious dogs. Nicotine produced a non-significant decrease in enkephalin levels. These observations suggest that there are interactions between endogenous opioid and nicotinic processes. However, they are complex and may differ from one functional system to another.
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PMID:Interaction between nicotine and endogenous opioid mechanisms in the unanesthetized dog. 717 83

Following central nervous system insults, control of intracranial pressure may lessen the incidence of morbidity and mortality. Therapies to control intracranial pressure include osmolar agents, prevention of and control of seizures, drainage of cerebrospinal fluid, hypothermia, and barbiturates. Control of agitation and excessive patient movement are additional components in the management of ICP. Although opioids and benzodiazepines are generally effective, in a small subset of patients, alternative agents may be necessary. The authors present 2 children with increased ICP in whom propofol was used to provide sedation and control ICP. The use of propofol in this setting and its possible applications in the children with increased ICP are discussed.
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PMID:Propofol for sedation and control of intracranial pressure in children. 1070 29

Acute liver failure (ALF) is an uncommon medical emergency whose rapid progression and high mortality demand early diagnosis and expert management, including immediate transfer of any potential case to facilities for intensive care and orthotopic liver transplantation (OLT). All patients with ALF must be screened aggressively for acetaminophen toxicity (history, serum levels, "hyperacute" presentation with renal failure), for other drugs, and viral hepatitis; rare causes of ALF should also be considered. After an acetaminophen overdose, N-acetylcysteine must be given as early as possible, preferably in the emergency room, but any patient with ALF should promptly receive N-acetylcysteine if there is suspicion of acetaminophen toxicity irrespective of the time of ingestion. Supportive care for all patients with ALF includes adequate enteral nutrition, aggressive screening and treatment of infection, prophylactic broad-spectrum antibiotics, and antifungal agents. Sedation with propofol is given for severe agitation or mechanical ventilation. With advanced coma grades, intensive care is needed with hemodynamic monitoring, ventilatory support, continuous renal replacement for renal failure, and intracranial pressure monitoring. Intracranial hypertension is treated with mannitol and/or acute short-term hyperventilation, but if the patient is refractory to treatment, mild-moderate hypothermia is achieved by a cooling blanket that is continued throughout OLT. Barbiturate coma is only used in refractory cases as the last treatment modality. Seizures are aggressively treated with phenytoin, with additional diazepam as needed. Candidacy and activation for OLT should be completed as early as possible in the course of ALF, especially in "hyperacute" cases such as acetaminophen toxicity. The final decision to proceed with OLT is made when a donor organ becomes available. King's College Hospital criteria for OLT are still the best prognostic assessment for fatal outcome in ALF, but the criteria fail to identify some patients who will die.
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PMID:Acute Liver Failure. 1552 12

Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested as a natural animal model of human depression and mood disorders.
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PMID:Metabolic depression in hibernation and major depression: an explanatory theory and an animal model of depression. 1606 29

Cardiopulmonary resuscitation does not end with restoration of spontaneous circulation; rather, it must be continued with the application of all the measures that allow organ function to be maintained. The initial goal of hemodynamic treatment is to achieve normal blood pressure for the patient's age by means of fluids and/or vasoactive drugs. The aim of respiratory treatment is to normalize ventilation and oxygenation without causing further lung injury, avoiding hyperoxia and hyperventilation as well as hypoxia and hypercapnia. Neurological stabilization aims to reduce secondary brain damage, by avoiding hypertension and hypotension, maintaining normal ventilation and oxygenation, and treating hyperglycemia, agitation and seizures. Although no specific studies in children are available, data from adults have shown that early moderate hypothermia attenuates brain damage secondary to cardiorespiratory arrest, without increasing complications. After the arrest, the need for analgesia and/or sedation must be considered. The process of transportation to the pediatric intensive care unit (PICU) requires the following steps: stabilizing the patient, checking for and stabilizing fractures and external wounds, ensuring a stable airway and intravenous lines, assessing the need for nasogastric and bladder tubes, taking blood samples for analyses, contacting the PICU and informing the staff about the child's condition, choosing the optimal vehicle for transportation according to the child's condition and the distance, checking pediatric equipment and medications, selecting experienced staff and, finally, maintaining close surveillance and monitoring during transportation.
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PMID:[Post-resuscitation stabilization and transportation]. 1734 Jul 87

Sedation-analgesia occupies an essential place in the specific therapeutic arsenal of the brain-injured patients. The maintenance of the perfusion of the brain, its relaxation and its protection are the fundamental objectives whose finality is to avoid the extension of the lesions and to preserve the neuronal capital. Sedation is instituted when patients are severely agitated or present a deterioration of their state of consciousness (GCS< or =8). Under cover of mechanical ventilation, sedation is the first line treatment of intracranial hypertension, a common pathway of various acute brain diseases of traumatic, vascular or other origin. The use of the combination of hypnotic and opioids is the rule. The combined action of these two classes reinforces and improves their sedative effects. Midazolam is the 2 benzodiazepine of reference. Propofol is more and more frequently added to the combination of hypnotic and opioids. The "propofol infusion syndrome" is a severe limitation to its long term administration in particular among patients presenting a severe septic or inflammatory state. Propofol will be imperatively stopped in the event of metabolic acidosis, rhabdomyolysis, acute renal insufficiency, hyperkaliemia or increase in the blood triglyceride levels. The use of thiopental is restricted to the most severe cases. Its use as a monotherapy at high doses is abandoned to the profit of a co-administration with midazolam or even with the combination of midazolam and propofol. Thiopental overdose is very frequent in the event of associated hypothermia. Etomidate does not have its place apart from induction in fast sequence. The neuro-protective effects of ketamine require to be demonstrated in man before being recommended routinely. Withdrawal of sedation can be responsible for a state of agitation which can be controlled by neuroleptics.
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PMID:[Sedation and analgesia for the brain-injured patient]. 1861 62

Dexmedetomidine is a centrally acting alpha2-adrenergic agonist which is currently Food and Drug Administration-approved for the short-term (less than 24 hours) sedation of adults during mechanical ventilation. Given its beneficial physiologic effects and limited adverse effect profile, there is growing interest regarding its potential applications in the Pediatric intensive care unit patient including sedation during mechanical ventilation, procedural sedation, the treatment of withdrawal, and prevention of emergence agitation. Although generally safe and effective, occasional hemodynamic effects including bradycardia and hypotension have been reported. Clinical experience has demonstrated that bradycardia may be more common when dexmedetomidine is administered with other medications that have negative chronotropic effects. We report 2 pediatric patients with traumatic brain injury who had good long-term neurologic outcomes, but developed clinically significant bradycardia when therapeutic hypothermia was added to a sedation regimen that included dexmedetomidine and remifentanil. The role of dexmedetomidine as a neuroprotective agent is explored as well as a review presented of previous reports of bradycardia related to dexmedetomidine.
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PMID:Bradycardia during dexmedetomidine and therapeutic hypothermia. 1879 67

The objective of this study was to identify the prevalent complications in the postanesthesia recovery room (PARR), and correlate nurses' work hours with the complications. The sample consisted of 400 records of patients older than 18 years, who had major and medium surgical procedures, admitted at the PARR unit, with a stay of at least one hour. The prevalent complications were pain and hypothermia. The following complications showed a statistically significant relationship with the nursing intervention: pain: routine, oxygen therapy, medication and bandages; agitation/anxiety: routine and oxygen therapy; hypotension: hydration, complementary exams, and observation; hypertension: observation; tremor: mat heater, blood transfusion; nausea/vomiting: routine, medication and urinary catheterization; bleeding: routine, medication and bandages; hypoxemia: routine and oxygen therapy; hypothermia: routine, mat heater, and medication. Pain, nausea/vomiting, agitation and bleeding showed a statistically significant relationship with the PARR nurse.
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PMID:[Nurse interventions and the complications in the post-anesthesia recovery room]. 2008 69

p-Synephrine is an adrenergic amine found in Citrus aurantium L. fruits and has been used for weight loss in dietary supplements. There are commercial products containing this substance associated to caffeine, salicin, and ephedrine. The aim of this study was to evaluate the acute toxicity of this mixture in mice of both sexes. The significative results observed after acute oral administration to male and female mice of 300, 350, and 400 mg/kg total of p-synephrine, ephedrine, salicin, plus caffeine in a 10:4:6:80 w/w ratio included a reduction in locomotor activity and ptosis in all treated groups for both sexes. Seizures were also observed in male (400 mg/kg) and female groups (350 and 400 mg/kg). Gasping and tearing were observed in males. Salivation (400 mg/kg), agitation (350 and 400 mg/kg), and piloerection (all treated groups) were significantly observed only in females. Deaths occurred in males at 350 and 400 mg/kg treated groups and the necropsy showed cardiopulmonary hemorrhage. A reduction in locomotor activity was confirmed through the spontaneous locomotor activity test, in which the number of crossings considerably decreased (P < .01) in all treated groups. The rotarod test showed a decrease in motor coordination at 400 mg/kg. Body temperature decreased significantly (P < .01) in all treated groups compared to controls. The results suggested clear signs of toxicity of p-synephrine, ephedrine, salicin, and caffeine association; this toxicity augments the attentiveness on commercial products containing this mixture, given the expressive number of adverse events related to its utilization.
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PMID:Toxicological effects of a mixture used in weight loss products: p-synephrine associated with ephedrine, salicin, and caffeine. 2240 69


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