The Febrile Infant

1979 ◽  
Vol 1 (2) ◽  
pp. 35-36
Author(s):  
ARNOLD L. SMITH
Keyword(s):  
Blood Flow ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Fundamental Goal ◽  
Febrile Infant ◽  
Abnormal Increase ◽  
The Face ◽  
Sorting Process ◽  
Core Body ◽  
Body Heat

Sorting out the child at risk, from those with illness that is not a threat to their health, is a fundamental goal of pediatrics. One of the most common complaints, which prompts us to initiate the sorting process, is fever. In the article by McCarthy (p 51), guidelines to aid in the sorting process are suggested. Fever, an abnormal increase in core body temperature, results primarily from a decrease in heat loss; decreased trunk and extremity skin blood flow decreases the surface area available for convection and body heat loss decreases—mom feels the forehead or the face for increased temperature, areas less affected by thermoregulatory vasoconstriction.

scholarly journals Temperature Monitoring and Perioperative Thermoregulation

2008 ◽  
Vol 109 (2) ◽  
pp. 318-338 ◽  
Author(s):  
Daniel I. Sessler ◽  
David S. Warner ◽  
Mark A. Warner
Keyword(s):  
Body Temperature ◽  
General Anesthesia ◽  
Core Temperature ◽  
Core Body Temperature ◽  
Neuraxial Anesthesia ◽  
General Anesthetics ◽  
The Core ◽  
Core Body ◽  
Dose Dependent ◽  
Body Heat

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.

Infrared thermal imaging as a method to study thermogenesis in the neonatal lamb

2014 ◽  
Vol 54 (9) ◽  
pp. 1497 ◽  
Author(s):  
S. A. McCoard ◽  
H. V. Henderson ◽  
F. W. Knol ◽  
S. K. Dowling ◽  
J. R. Webster
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Cold Exposure ◽  
Thermal Imaging ◽  
Core Body Temperature ◽  
Recovery Period ◽  
Exposure Period ◽  
Skin Surface ◽  
Infrared Thermal Imaging ◽  
Core Body

The combination of heat generation and reducing heat loss from the skin surface is important for maintaining core body temperature in a neonate. Thermogenesis studies traditionally focus on measurement of core body temperature but not the contribution of radiated heat loss at the skin surface. This study aimed to evaluate the utility of using thermal imaging to measure radiated heat loss in newborn lambs. Continuous thermal images of newborn lambs were captured for 30 min each during the baseline (11−18°C), cold-exposure (0°C) and recovery (11−18°C) periods by using an infrared camera. Core body temperature measured by rectal thermometer was also recorded at the end of each period. In all, 7 of the 10 lambs evaluated had reduced rectal temperatures (0.4−1°C) between the baseline and recovery periods, while three maintained body temperature despite cold exposure. During the baseline period, infrared heat loss was relatively stable, followed by a rapid decrease of 5°C within 5 min of cold exposure. Heat loss continued to decrease linearly in the cold-exposure period by a further 10°C, but increased rapidly to baseline levels during the recovery period. A temperature change of between 20°C and 35°C was observed during the study, which was likely to be due to changes in vasoconstriction in the skin to conserve heat. The present study has highlighted the sensitivity of infrared thermal imaging to estimate heat loss from the skin in the newborn lamb and shown that rapid changes in heat loss occur in response to cold exposure.

Do chronic primary insomniacs have impaired heat loss when attempting sleep?

2006 ◽  
Vol 290 (4) ◽  
pp. R1115-R1121 ◽  
Author(s):  
Michael Gradisar ◽  
Leon Lack ◽  
Helen Wright ◽  
Jodie Harris ◽  
Amber Brooks
Keyword(s):  
Skin Temperature ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Finger Skin Temperature ◽  
Finger Temperature ◽  
Temperature Changes ◽  
The Core ◽  
Hands And Feet ◽  
Core Body ◽  
Finger Skin

For good sleepers, distal skin temperatures (e.g., hands and feet) have been shown to increase when sleep is attempted. This process is said to reflect the body’s action to lose heat from the core via the periphery. However, little is known regarding whether the same process occurs for insomniacs. It would be expected that insomniacs would have restricted heat loss due to anxiety when attempting sleep. The present study compared the finger skin temperature changes when sleep was attempted for 11 chronic primary insomniacs [mean age = 40.0 years (SD 13.3)] and 8 good sleepers [mean age = 38.6 years (SD 13.2)] in a 26-h constant routine protocol with the inclusion of multiple-sleep latency tests. Contrary to predictions, insomniacs demonstrated increases in finger skin temperature when attempting sleep that were significantly greater than those in good sleepers ( P = 0.001), even though there was no significant differences in baseline finger temperature ( P = 0.25). These significant increases occurred despite insomniacs reporting significantly greater sleep anticipatory anxiety ( P < 0.0008). Interestingly, the core body temperature mesor of insomniacs (37.0 ± 0.2°C) was significantly higher than good sleepers (36.8 ± 0.2°C; P = 0.03). Whether insomniacs could have impaired heat loss that is masked by elevated heat production is discussed.

Bombesin-Induced Hypothermia in the Insulin-Treated Rat: Effect on Tail-Skin Temperature

1989 ◽  
Vol 69 (3-2) ◽  
pp. 1339-1345
Author(s):  
Alex M. Babcock ◽  
Chris Barton
Keyword(s):  
Central Nervous System ◽  
Skin Temperature ◽  
Heat Loss ◽  
Preoptic Area ◽  
Core Body Temperature ◽  
Induced Hypothermia ◽  
Autonomic Functions ◽  
Core Body ◽  
Skin Temperatures ◽  
Intrahypothalamic Injection

Bombesin-like peptides are widely distributed in the mammalian central nervous system and appear to participate in the regulation of a variety of autonomic functions. Bombesin has been shown to alter feeding behavior, locomotor activity, and thermoregulation. Microinfusion of bombesin into the preoptic area of the hypothalamus produces a reduction in core body temperature, but only if the rat has been cold-exposed, food-deprived, or pretreated with insulin. The mechanism for bombesin-induced hypothermia under the latter two conditions is unknown. The present study evaluated the possible contribution of peripheral heat loss mechanisms in bombesin-induced hypothermia. Rats were administered insulin (10U/kg, Regular Iletin I i.m.) or saline followed by an intrahypothalamic injection of bombesin (.05 μg/ .25 μl) or peptide vehicle. Rectal and tail-skin temperatures were measured continuously for 120 min. Changes in temperature were evaluated at 30, 60, 90, and 120 min., using analysis of variance. As previously demonstrated, bombesin produced hypothermia in rats pretreated with insulin. This reduction in core temperature was not associated with any significant alteration in tail-skin temperature. Results suggest that bombesin-induced hypothermia in rats pretreated with insulin may not be mediated by an increase in peripheral heat loss.

scholarly journals Elevated body temperature during sleep in orexin knockout mice

2006 ◽  
Vol 291 (3) ◽  
pp. R533-R540 ◽  
Author(s):  
Takatoshi Mochizuki ◽  
Elizabeth B. Klerman ◽  
Takeshi Sakurai ◽  
Thomas E. Scammell
Keyword(s):  
Locomotor Activity ◽  
Body Temperature ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Biological Rhythms ◽  
Physiological Factors ◽  
Sustained Activity ◽  
Recovery Sleep ◽  
Core Body ◽  
Elevated Body Temperature

Core body temperature (Tb) is influenced by many physiological factors, including behavioral state, locomotor activity, and biological rhythms. To determine the relative roles of these factors, we examined Tb in orexin knockout (KO) mice, which have a narcolepsy-like phenotype with severe sleep-wake fragmentation. Because orexin is released during wakefulness and is thought to promote heat production, we hypothesized that orexin KO mice would have lower Tb while awake. Surprisingly, Tb was the same in orexin KO mice and wild-type (WT) littermates during sustained wakefulness. Orexin KO mice had normal diurnal variations in Tb, but the ultradian rhythms of Tb, locomotor activity, and wakefulness were markedly reduced. During the first 15 min of spontaneous sleep, the Tb of WT mice decreased by 1.0°C, but Tb in orexin KO mice decreased only 0.4°C. Even during intense recovery sleep after 8 h of sleep deprivation, the Tb of orexin KO mice remained 0.7°C higher than in WT mice. This blunted fall in Tb during sleep may be due to inadequate activation of heat loss mechanisms or sustained activity in heat-generating systems. These observations reveal an unexpected role for orexin in thermoregulation. In addition, because heat loss is an essential aspect of sleep, the blunted fall in Tb of orexin KO mice may provide an explanation for the fragmented sleep of narcolepsy.

Role of the hypothalamic PVN in the reflex reduction in mesenteric blood flow elicited by hyperthermia

2008 ◽  
Vol 295 (6) ◽  
pp. R1874-R1881 ◽  
Author(s):  
Feng Chen ◽  
Melissa Dworak ◽  
Yuliang Wang ◽  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Separate Group ◽  
Control Group ◽  
Mesenteric Blood Flow ◽  
Significant Difference ◽  
Core Body

The hypothalamic paraventricular nucleus (PVN) is an important integrative center in the brain. In the present study, we investigated whether the PVN is a key region in the mesenteric vasoconstriction that normally accompanies an increase in core body temperature. Anesthetized rats were monitored for blood pressure, heart rate, mesenteric blood flow, and vascular conductance. In control rats, elevation of core body temperature to 41°C had no significant effect on blood pressure, increased heart rate, and reduced mesenteric blood flow by 21%. In a separate group of rats, muscimol was microinjected bilaterally (1 nmol/side) into the PVN. Compared with the control group, there was no significant difference in the blood pressure and heart rate responses elicited by the increase in core body temperature. In contrast to control animals, however, mesenteric blood flow did not fall in the muscimol-treated rats in response to the elevation in core body temperature. In a separate group, in which muscimol was microinjected into regions outside the PVN, elevating core body temperature elicited the normal reduction in mesenteric blood flow. The results suggest that the PVN may play a key role in the reflex decrease in mesenteric blood flow elicited by hyperthermia.

Disturbance of thermal homeostasis following dynamic exercise

2007 ◽  
Vol 32 (4) ◽  
pp. 818-831 ◽  
Author(s):  
Glen P. Kenny ◽  
Ollie Jay ◽  
W. Shane Journeay
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Dynamic Exercise ◽  
Hemodynamic Changes ◽  
Post Exercise ◽  
Cutaneous Vasodilation ◽  
Baseline Values ◽  
Sudomotor Activity ◽  
Core Body

Recovery from dynamic exercise results in significant perturbations of thermoregulatory control. These perturbations evoke a prolonged elevation in core body temperature and a concomitant decrease in sweating, skin blood flow, and skin temperature to pre-exercise baseline values within the early stages of recovery. Cutaneous vasodilation and sweating are critical responses necessary for effective thermoregulation during heat stress in humans. The ability to modulate the rate of heat loss through adjustments in vasomotor and sudomotor activity is a fundamental mechanism of thermoregulatory homeostasis. There is a growing body of evidence in support of a possible relationship between hemodynamic changes postexercise and heat loss responses. Specifically, nonthermoregulatory factors, such as baroreceptors, associated with hemodynamic changes, influence the regulation of core body temperature during exercise recovery. The following review will examine the etiology of the post-exercise disturbance in thermal homeostasis and evaluate possible thermal and nonthermal factors associated with a prolonged hyperthermic state following exercise.

A relationship between heat loss and sleepiness: effects of postural change and melatonin administration

1997 ◽  
Vol 83 (1) ◽  
pp. 134-139 ◽  
Author(s):  
Kurt Kräuchi ◽  
Christian Cajochen ◽  
Anna Wirz-Justice
Keyword(s):  
Heat Loss ◽  
Core Body Temperature ◽  
Circadian System ◽  
Postural Change ◽  
Melatonin Administration ◽  
Postural Changes ◽  
Subjective Sleepiness ◽  
Core Body ◽  
Skin Temperatures ◽  
Lying Down

Kräuchi, Kurt, Christian Cajochen, and Anna Wirz-Justice. A relationship between heat loss and sleepiness: effects of postural change and melatonin administration. J. Appl. Physiol. 83(1): 134–139, 1997.—Both the pineal hormone melatonin (Mel) and postural changes have thermoregulatory sequelae. The purpose of the study was to evaluate their relationship to subjective sleepiness. Eight healthy young men were investigated under the unmasking conditions of a constant routine protocol. Heart rate, rectal temperature (Tre), skin temperatures (foot, Tfo; and stomach), and subjective sleepiness ratings were continuously recorded from 1000 to 1700. Mel (5 mg po) was administered at 1300, a time when Mel should not phase shift the circadian system. Both the postural change at 1000 from upright to a supine position (lying down in bed) and Mel administration at 1300 reduced Treand increased Tfo in parallel with increased sleepiness. These findings suggest that under comfortable ambient temperature conditions, heat loss via the distal skin regions (e.g., feet) is a key mechanism for induction of sleepiness as core body temperature declines.

scholarly journals Nitric oxide and fever: immune-to-brain signaling vs. thermogenesis in chicks

2016 ◽  
Vol 310 (10) ◽  
pp. R896-R905 ◽  
Author(s):  
Valter Dantonio ◽  
Marcelo E. Batalhão ◽  
Marcia H. M. R. Fernandes ◽  
Evilin N. Komegae ◽  
Gabriela A. Buqui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Core Body Temperature ◽  
No Synthase ◽  
High Dose ◽  
Compensatory Mechanisms ◽  
The Face ◽  
Plasma Nitrate ◽  
Synthase Inhibitor ◽  
Core Body ◽  
The Brain

Nitric oxide (NO) plays a role in thermogenesis but does not mediate immune-to-brain febrigenic signaling in rats. There are suggestions of a different situation in birds, but the underlying evidence is not compelling. The present study was designed to clarify this matter in 5-day-old chicks challenged with a low or high dose of bacterial LPS. The lower LPS dose (2 μg/kg im) induced fever at 3–5 h postinjection, whereas 100 μg/kg im decreased core body temperature (Tc) (at 1 h) followed by fever (at 4 or 5 h). Plasma nitrate levels increased 4 h after LPS injection, but they were not correlated with the magnitude of fever. The NO synthase inhibitor ( NG-nitro-l-arginine methyl ester, l-NAME; 50 mg/kg im) attenuated the fever induced by either dose of LPS and enhanced the magnitude of the Tc reduction induced by the high dose in chicks at 31–32°C. These effects were associated with suppression of metabolic rate, at least in the case of the high LPS dose. Conversely, the effects of l-NAME on Tc disappeared in chicks maintained at 35–36°C, suggesting that febrigenic signaling was essentially unaffected. Accordingly, the LPS-induced rise in the brain level of PGE2 was not affected by l-NAME. Moreover, l-NAME augmented LPS-induced huddling, which is indicative of compensatory mechanisms to run fever in the face of attenuated thermogenesis. Therefore, as in rats, systemic inhibition of NO synthesis attenuates LPS-induced fever in chicks by affecting thermoeffector activity and not by interfering with immune-to-brain signaling. This may constitute a conserved effect of NO in endotherms.

Functional link between distal vasodilation and sleep-onset latency?

2000 ◽  
Vol 278 (3) ◽  
pp. R741-R748 ◽  
Author(s):  
Kurt Kräuchi ◽  
Christian Cajochen ◽  
Esther Werth ◽  
Anna Wirz-Justice
Keyword(s):  
Heat Loss ◽  
Core Body Temperature ◽  
Sleep Onset ◽  
Predictor Variable ◽  
Rapid Onset ◽  
Rate Of Change ◽  
Sleep Onset Latency ◽  
Onset Latency ◽  
Functional Link ◽  
Core Body

Thermoregulatory processes have long been implicated in initiation of human sleep. The purpose of this study was to evaluate the role of heat loss in sleep initiation, under the controlled conditions of a constant-routine protocol modified to permit nocturnal sleep. Heat loss was indirectly measured by means of the distal-to-proximal skin temperature gradient (DPG). A stepwise regression analysis revealed that the DPG was the best predictor variable for sleep-onset latency (compared with core body temperature or its rate of change, heart rate, melatonin onset, and subjective sleepiness ratings). This study provides evidence that selective vasodilation of distal skin regions (and hence heat loss) promotes the rapid onset of sleep.

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