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Temperature taking--getting it right.

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S Brown. 1990-12-12. Temperature taking--getting it right.. https://doi.org/10.7748/ns.5.12.4.s61

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Influence of fever on the hypermetabolic response in burn-injured children.

BACKGROUND: Burn injury typically elicits a hypermetabolic response characterized by increased energy expenditure and muscle protein catabolism. HYPOTHESIS: Fever further increases energy expenditure and muscle loss in otherwise highly hypermetabolic burn patients. DESIGN: Retrospective analysis of experimental study. SETTING: University hospital. PATIENTS: Eighty-four children (aged 2-18 years) with burns covering 40% or more of total body surface area. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Simultaneous measurements of indirect calorimetry and leg net balance of phenylalanine (as an index of muscle protein catabolism) were obtained. Patients were stratified by their rectal temperature taken at the time of these metabolic measurements: afebrile (n = 28; temperature, <39.0 degrees C); mild fever (n = 26; temperature, 39.0 degrees C-39.4 degrees C); moderate fever (n = 18; temperature, 39.5 degrees C-39.9 degrees C); or severe fever (n = 12; temperature, > or =40.0 degrees C). RESULTS: Febrile and afebrile patients were similar in age, body weight, and extent of burn area. Severe fever was associated with significantly increased resting energy expenditure (mean +/- SD resting energy expenditure-predicted basal, 1.38 +/- 0.39 for afebrile patients vs 1.68 +/- 0.30 for patients with severe fever; P<.05) and a greater net loss of phenylalanine from the leg (net balance of phenylalanine, -6.0 +/- 6.2 mg/min per 100 mL of leg volume for afebrile patients vs -10.8 +/- 7.2 mg/min per 100 mL for patients with severe fever; P<.05). Patient groups were similar in plasma glucose concentration and extent of leukocytosis. CONCLUSIONS: These findings demonstrate the association of severe fever with further increase in energy expenditure and muscle protein catabolism in otherwise hypermetabolic burned children. This suggests a possible metabolic benefit in attenuating fever in such patients.

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The purpose of this study was to determine the effect of mild hypothermia on cerebral ischaemia due to severe vasospasm, which was refractory to medical and intravascular treatments and to assess the brain protection of this treatment in patients who underwent delayed aneurysm clipping after presenting with ischaemic neurological deficits. Mild hypothermia (32-34 degrees C of brain temperature) was employed in two groups: (1) Patients (Hunt and Kosnik grades I to II) who showed progressive neurological deficits due to vasospasm and did not respond to conventional therapy (Group 1) and (2) Patients who received delayed aneurysm clipping after presenting with ischaemic neurological deficits due to vasospasm (Group 2). Seven of 8 patients in both Groups showed a favorable outcome with mild hypothermia (good recovery in 5 and moderate disability in two patients). Mild hypothermia is considered to be effective on critical cerebral ischaemia due to vasospasm even after failure to response the conventional therapies and to provide brain protection in delayed aneurysm clipping.

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