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

Early and efficient management of severely burned patients facilitates outcome improvement. Pre-hospital care includes fluid loading with 2 mL.kg-1/% burn over the first six hours, sedation and analgesia, prevention of hypothermia and ventilatory support for either critically burned patients or facial, cervical or pulmonary burn injury. The transient stay in a general hospital before transfer to a burn centre allows extension of initial care, the critical investigation for associated injuries (intoxication, multiple trauma) and to perform initial local treatment with sterile coverage or vaseline gauze after a revised assessment of the burned skin area, and possibly escharotomies. The main aim of care in the burn centre is to control hypovolaemia and to obtain maximal tissue perfusion and oxygen delivery to burned tissues, as well as to healthy organs. To manage the burn shock (initially hypovolemic and later on hyperdynamic) catecholamines are often indicated when appropriate fluid loading remains insufficient. Mechanical ventilation is indicated in case of either a deep extensive burn over 60% of total body surface area, or facial and cervical burns or severe pulmonary burn injury from smoke inhalation, carbon monoxide intoxication, tracheobronchial thermal injury and blast injury. Because of the severity of burn-related pain, and the stimulus linked to intensive care, continuous sedation is usually required. Early surgical treatment such as escharotomies, excision and grafting, which cause significant pain as well as blood loss, and hydrotherapy, often require general anaesthesia. Burn injury can modify the volume of distribution and the pharmacokinetics of anaesthetic agents. Finally, chemical or electrical burn, radiation, associated CO intoxication or multiple trauma, as well as burn injury in infants, raise specific problems. With improvement in early intensive care, the survival rate of the most severely burned patients is obviously improving. New techniques in skin substitution will probably further improve the final outcome.
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PMID:[Management of severe burns during the 1st 72 hours]. 975 May 81

Recent advances in surgical techniques, control of infection and nutritional support have dramatically increased the survival rates of burned children. The characteristics of severely burned pediatric patients dictate that management be different from that required for adults in the intensive care unit. The formulas for fluid replacement should be based on body surface rather than weight in children and adjusted for degree of stress and age, with appropriate monitoring and treatment of hypothermia, pain and associated psychological disorders. Early assessment and treatment of airway obstruction and gas and smoke inhalation syndromes with high FiO2 is necessary; prophylactic endotracheal intubation may be required.
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PMID:[Resuscitation of the burned child in critical condition]. 978 Jul 65

Frostbite injuries occur mainly in toes, fingers, ears, nose and cheek. Typically an initial vasoconstriction in the skin will protect from drop in core temperature. Ice crystal development occurs when tissue temperature drops to -2 degrees C, leading to increased osmolality of the extracellular fluid and intracellular dehydration. An additional insult occurs with thawing due to reperfusion of the tissue and thereby release of inflammatory mediators. Symptoms of frostbite injury are: White-cyanotic discoloration, pain and numbness followed by hypoaesthesia. General hypothermia should be prevented and treated before managing the local frostbite injuries. Direct contact with warm skin without rubbing should be used in superficial injuries. More severe and deeper injuries should not be thawed until definite treatment could be given in a hospital. Re-freezing and mechanical influence on the injured parts must be avoided. Thawing should preferably be done in stirred water of 40-42 degrees C with mild soap. Antibiotics may be indicated when the skin barrier is broken. Surgical debridement should be postponed until a clear demarcation occurs.
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PMID:[Frostbite injuries]. 1007 36

Hypothermia results in diminished voluntary muscle activity, and is frequently used as a means of providing deep anesthesia to ectotherms and some mammals. In ectotherms, however, it is unclear if hypothermia produces true pain insensation. A needle-probe thermometer was used to demonstrate in frogs (Rana pipiens) that local hypothermia (9 degrees C) could be induced by placement of a tourniqueted leg into ice water (6 degrees C) for 10 min in contrast to the contralateral nontourniqueted leg (21.8 degrees C) kept out of ice water. Analgesia was tested by placement of dilutions of acetic acid on the rear leg. Further tests using groups of 10 frogs demonstrated that frogs with local hypothermia tolerated greater concentrations of acetic acid (mean acetic acid test score = 11) than morphine (10 mg/kg)-treated (9.6) or nontreated (5.8) frogs. Additional studies showed that morphine analgesia was blocked with naloxone doses as low as 0.01 mg/kg and hypothermia-induced analgesia at 10 mg/kg. Naltrexone blocked morphine analgesia at dosages as low as 0.01 mg/kg and hypothermia-induced analgesia at 0.10 mg/kg. In summary, this study demonstrates that hypothermia induces significant analgesia in an amphibian, and that this analgesia is partially blocked by naloxone and naltrexone, suggesting that the effect is mediated at least partially by opioid receptors.
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PMID:Evaluation of hypothermia-induced analgesia and influence of opioid antagonists in leopard frogs (Rana pipiens). 1034 May 22

Ginsenoside Rc, Rd, and Re induced antinociception in writhing and formalin tests among five representative ginsenosides: Rb1, Rc, Rd, Re, and Rg1. However, these ginsenosides had no effect in the tail-flick test. The antinociceptive effects induced by three ginsenosides were dose dependent. ED50 was 20.5 (7.3-57.4 mg/kg) for Rc, 17 (11.0-27.6 mg/kg) for Rd, and 3.5 (1-12 mg/ kg) for Re in the writhing test and 62 (42-90 mg/kg) for Rc, 45 (20.5-99.0 mg/kg) for Rd, and 82 (48-139 mg/kg) for Re in the second phase of the formalin test. The antinociceptive effects were not blocked by the opioid receptor antagonist naloxone in the writhing and formalin tests. These three ginsenosides did not affect motor function. Ginsenoside Rc and Rd induced hypothermia for 30 to 60 min, and ginsenoside Rc induced hyperthemia after 150 min of treatment at doses of 100 mg/kg. These results suggest that ginsenosides such as Rc, Rd, or Re inhibit mainly chemogenic pain rather than thermal pain by the nonopioid system in mice.
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PMID:Ginsenosides that produce differential antinociception in mice. 1040 90

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.
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PMID:Perioperative heat balance. 1069 Dec 47

Ischemic cerebrovascular diseases are commonly induced by atherosclerosis and cardiogenic embolization but rarely they occur in association with Takayasu's arteritis and aortic lesion such as aortic dissection and aneurysm. Here we experienced two cases of acute aortic disease complicated by ischemic cerebrovascular disease (CVD). Patient 1 was a 77-year-old male. He complained of dyspnea and left hemiparesis. He was brought to our hospital by ambulance. Left hemiparesis and dyspnea improved soon. The patient only complained of left lower extremity pain and physical examination revealed hypotension. Brain CT showed no abnormality but chest CT revealed aortic dissection. The resection of the intimal tear and replacement of ascending aorta and aortic arch with 28 mm Hemashield graft were performed under hypothermia and selective cerebral perfusion. The postoperative course was uneventful and he has been doing well. Patient 2 was a 67-year-old female. She was found lying unconscious and brought to our hospital by ambulance. Physical examination revealed right hemiparesis and hypotension. Brain CT demonstrated low density area in the left corona radiata and ruptured aortic aneurysm was seen in abdominal CT. Just after the examination, the patient suddenly complained of severe back pain and died despite cardiopulmonary resuscitation. Aortic lesions can manifest ischemic symptom involving multiple organs following their vascular disorder. Aortic dissection rarely occurs in association with ischemic CVD and in that case it is likely to be seen by neurologists. Aortic dissection and aneurysm deteriorate so suddenly that immediate diagnosis and proper treatment are needed.
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PMID:[Two cases of acute aortic disease complicated by ischemic cerebrovascular disease]. 1076 48

The present study directly compared the antinociceptive and toxic effects of the neuronal nicotinic receptor agonist ABT-594 ((R)-5-(2-azetidinylmethoxy)-2-chloropyridine) with (-)-nicotine and (+)-epibatidine. Like (-)-nicotine (0.8 and 1.6 mg/kg s.c.) and (+)-epibatidine (0.005 and 0.01 mg/kg s.c.), ABT-594 (0.05 and 0.1 mg/kg s.c.) increased response latencies in the hot-plate test in rats, indicating that it has antinociceptive activity. In contrast to (-)-nicotine and (+)-epibatidine, ABT-594 did not cause rotarod impairment at antinociceptive doses but did cause hypothermia and life-threatening adverse effects including seizures. ABT-594 (0.01 and 0.1 mg/kg i.v.) also produced a dose-dependent increase in blood pressure resembling that observed with (-)-nicotine (0.03, 0.1 and 0. 03 mg/kg i.v.) and (+)-epibatidine (0.001 and 0.003 mg/kg i.v.). Both the antinociceptive and toxic effects (convulsions and hypertension) were abolished by pretreatment with the brain penetrant neuronal nAChR antagonist mecamylamine (1 mg/kg s.c.; i.v. for cardiovascular studies), demonstrating that these actions of ABT-594 were mediated via activation of neuronal nicotinic receptors. Continuous infusion of ABT-594 (0.2 mg/kg per day s.c.) to rats for 7 days followed by challenge with mecamylamine (1 mg/kg i.p.) induced a nicotine-like abstinence syndrome suggesting that ABT-594 has nicotine-like dependence liability. These findings indicate that the acute safety profile of ABT-594 is not significantly improved over other nicotinic analgesics.
Pain 2000 Apr
PMID:Analgesic and toxic effects of ABT-594 resemble epibatidine and nicotine in rats. 1078 17

This study examined the ability of the anti-opioid Neuropeptide FF (NPFF) to modify the endogenous activity of nitric oxide (NO). Antinociceptive and hypothermic effects of 1DMe (D.Tyr-Leu-(n.Me)Phe-Gln-Pro-Gln-Arg-Phe-NH(2)), an NPFF agonist, and of L-NAME (N(omega)nitro-L-arginine methyl ester), an inhibitor of nitric oxide synthase, were investigated in mice. Intraperitoneal (i.p.) injection of L-NAME induced, in the hot plate test, a dose-dependent antinociception not reversed by naloxone, an opioid antagonist, but inhibited by L-Arg, the NO synthesis precursor. Intracerebroventricular (i.c.v.) injections of 1DMe inhibit the antinociceptive activity of L-NAME in a dose-dependent manner. On the contrary, L-NAME markedly potentiated hypothermia induced by 1DMe injected in the third ventricle. These data show that Neuropeptide FF receptors exert a dual effect on endogenous NO functions and could modulate pain transmission independently of opioids.
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PMID:Opposing interplay between Neuropeptide FF and nitric oxide in antinociception and hypothermia. 1103 7

This paper describes the phenomenon of post-anaesthetic shaking (PAS) as it is discussed in the literature. Literature was obtained via computerised searches of the Cochrane Library, Medline, and Cumulative Index of Nursing and Allied Health Literature (CINAHL) databases. This review considers PAS in adults, who have had either a general or regional anaesthetic. It focuses on the controversy regarding the cause of the condition, the role of anaesthetics in hypothermia, pharmacological interventions, and non-pharmacological interventions. The key conclusion to emerge is that nurses must take patients' shaking seriously and initiate treatment for it. If PAS is associated with hypothermia then the patient needs to be rewarmed, and if it is associated with pain, analgesia needs to be administered.
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PMID:Post-anaesthetic shaking. A review of the literature. 1122 7


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