Profound Hypothermia in Man

Niazi, Suad A.; Fj, Lewis

doi:10.1097/00000658-195802000-00019

Cited by 122 publications

(38 citation statements)

References 2 publications

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“…58 A survey of patients with stage IV hypothermia at one center showed that organ failure was common 24 hours after admission, and among fatal cases of organ failure, the most common cause of death was pulmonary edema. 3 Patients with primary hypothermia and cardiac stability who have been treated with active external and minimally invasive rewarming have a rate of neurologically intact survival of approximately 100%, 16 whereas for patients with cardiac arrest treated with extracorporeal rewarming, the rate is approximately 50%.…”

Section: Ou T C Omementioning

confidence: 99%

Accidental Hypothermia

et al. 2012

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A ccidental hypothermia (i.e., an involuntary drop in core body temperature to <35°C [95°F]) is a condition associated with significant morbidity and mortality. 1-4 Each year, approximately 1500 patients in the United States have hypothermia noted on their death certificate; however, the incidence of primary and secondary hypothermia and the associated morbidity and mortality remain unknown. 5 In a single tertiary care center, 14 different rewarming methods were used to treat 84 cases of accidental hypothermia, 3 which reflects the uncertainties about treatment and the potential for complications. 3 Certain treatment approaches are available only in specialized centers, and clarification is needed regarding the choice between transporting a patient to a specialized center and providing treatment locally. Existing recommendations do not include recent developments in rewarming methods nor do they assist with decisions regarding transportation. 6-8 PR E SEN TAT IONWith cold exposure, the initial response of the body is to maintain a normal core temperature (approximately 37°C [99°F]) by means of active movement and involuntary shivering. Primary hypothermia occurs when heat production in an otherwise healthy person is overcome by the stress of excessive cold, especially when the energy stores of the body are depleted. Secondary hypothermia can occur in ill persons with a wide variety of medical conditions (Table 1), even in a warm environment. Death in patients with secondary hypothermia is often caused by the underlying condition rather than by hypothermia. In all types of hypothermia, consciousness, breathing, and circulation are initially intact but are impaired as the body cools. 10

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Section: Ou T C Omementioning

confidence: 99%

Accidental Hypothermia

et al. 2012

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“…[16][17][18][19][20] Although many improvements have been introduced since the technique was first established, there remain recognized complications secondary to unique physiologic trespasses associated with HCA and CPB. [19][20][21][22] Further refinements of the technique require an appropriate experimental model.…”

Section: Discussionmentioning

confidence: 99%

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

Wang

Zheng

et al. 2006

Can J Anesth/J Can Anesth

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Purpose: This study tests the hypothesis that low hematocrit (Hct) worsens cerebral injury after prolonged hypothermic circulatory arrest (HCA) in rats, and the mechanism involves variable expression of the genes C-Fos, Bcl-2 and Bax.Methods: A rat HCA model was developed, and 40 animals were randomly assigned to four groups: Sham (sham) group, or Hct groups of Hct 10%, Hct 20% and Hct 30%. After 90 min of HCA at 18°C, physiologic variables were recorded and brain morphological changes were evaluated with light and electron microscopy. Expressions of C-Fos, Bcl-2, Bax in various brain areas were measured by the reverse transcriptase polymerase chain reaction and standard immunohistochemistry techniques. Results:The number of injured neurons in the hippocampus CA1 and parietal cortex in the Hct 10% group (CA1: 11.44 ± 2.52; cortex: 13.65 ± 2.31) exceeded the mean number of injured neurons in the Hct 20% group (CA1: 8.29 ± 1.31; cortex: 10.68 ± 1.24; P < 0.05) and the Hct 30% group. Mean mitochondrial injury scores were greatest at lower Hct levels, while the expression of C-Fos and Bax were highest in the Hct 10% group and lowest in the Hct30% group (P < 0.05). In contrast, the expression of the Bcl-2 mRNA was greatest in the Hct 30% group (P < 0.05). Conclusion:Low Hct worsens cerebral injury after prolonged HCA and CPB in rats, which may relate in part to the variable expression of the genes C-Fos, Bcl-2 and Bax. Hct 10 % (CA1: 11,44 ± 2,52; cortex: 13,65 ± 2,31) que dans le groupe Hct 20 % (CA1 : 8,29 ± 1,31 ; cortex : 10,68 ± 1,24 ; P < 0,05) Méthode : Un modèle d'ACH a été développé chez le rat et on a réparti de façon aléatoire 40 animaux dans quatre groupes : un groupe sans intervention et des groupes Hct de 10 %, 20 % et 30 %. Après un ACH pendant 90 min à 18°C, on a mesuré les variables physiologiques et on a évalué les changements morphologiques dans le cerveau avec la microscopie optique et électronique. On a mesuré l'expression de C-Fos, Bcl-2 et Bax dans différentes régions du cerveau par la réaction en chaîne transcriptase inverse -polymérase et par des techniques habituelles d'immunohistochimie. Résultats : Les neurones CA1 de l'hippocampe et du cortex pariétal ont été atteints en plus grand nombre dans le groupe

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“…HCA is an important technique for repair of complex congenital heart lesions and operations on the aortic arch and thoracic aorta [1–3]. It provides a bloodless operative field, unobstructed by vascular clamps and cannulae.…”

Section: Commentmentioning

confidence: 99%

“…Hypothermic circulatory arrest (HCA) was initially introduced for the repair of complex congenital heart lesions, but has since been widely adopted for aortic arch and thoracic aortic procedures [1–3]. It is a technique that affords the surgeon a bloodless operative field unobstructed by vascular clamps and cannulae.…”

Section: Introductionmentioning

confidence: 99%

Glutamate Excitotoxicity Mediates Neuronal Apoptosis After Hypothermic Circulatory Arrest

Tseng

Brock

Lange

et al. 2010

The Annals of Thoracic Surgery

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Background-Prolonged hypothermic circulatory arrest results in neuronal cell death and neurologic injury. We have previously shown that hypothermic circulatory arrest causes both neuronal apoptosis and necrosis in a canine model. Inhibition of neuronal nitric oxide synthase reduced neuronal apoptosis, while glutamate receptor antagonism reduced necrosis in our model. This study was undertaken to determine whether glutamate receptor antagonism reduces nitric oxide formation and neuronal apoptosis after hypothermic circulatory arrest.

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Profound Hypothermia in Man

Cited by 122 publications

References 2 publications

Accidental Hypothermia

Accidental Hypothermia

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

Glutamate Excitotoxicity Mediates Neuronal Apoptosis After Hypothermic Circulatory Arrest

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