Thermal balance and metabolic rate during upper respiratory tract infection in infants.

Abstract

Sequential recordings were made in the first five months after birth of metabolic rate, environmental temperature, and body temperature during sleep at home in 17 infants, each with an older sibling. Further recordings were made whenever an older sibling developed an upper respiratory tract infection (URTI), again four to six days later, and again two weeks later, aiming to achieve recordings before, during, and after an URTI in the infant. The temperature of the room and wrapping of the infant were determined according to their usual practice by the parents.Parents added appropriate wrapping to achieve thermal neutrality based on our calculated values and the measured oxygen consumption.In five of the six infants who developed an URTI in the first three months after birth there was no change or a decrease in metabolic rate at the time of the infection; for infants older than 3 months the metabolic rate increased in three of the five episodes recorded. Peripheral skin temperature decreased at the time of URTI at all ages, though in the older infants it usually increased in parallel with rectal temperature during the latter part of the night, when pyrexia was most common.Infants thus respond to URTI by heat conservation. In the younger infants the lower metabolic rate and the further decrease in this rate with URTI means that fever is rare, and their temperature may decrease on infection. In the older infants the increase in metabolic rate (from an already higher baseline) may result in fever. These differences may contribute to the increased vulnerability of the older infants to heat stress, particularly at the time of acute viral infections. (Arch Dis Child 1994; 70: 187-191) Thermal stress has been shown to be associated with an increased risk of sudden infant death syndrome (SIDS) in a number of anecdotal reports and in two case-control studies.' 2 Although the mechanism of such an association remains unclear, the reported effects of the thermal environment on respiratory pattern suggest that, at least in some subjects, the mechanism may involve an interaction between thermoregulation and respiratory control.3 In this context the head, as the site of about 40% of heat production and up to 85% of heat loss for the infant in bed, may be particularly vulnerable to the effects of thermal stress.4 In two studies an excess incidence of head covering was found in infants who died from SIDS compared with matched controls,5 6 and in animal studies relatively small changes in brain temperature have been shown to have potentially major effects on the control of respiration.7 Thus factors which increase the resting metabolic rate might have a significant influence on respiratory control both by a 'feed forward' effect of increased carbon dioxide production (which may directly affect respiratory drive) and by an effect on cerebral temperature, particularly under conditions (for example a prone sleeping position, head covering) in which the ability to lose heat from the head might be compromised.3 6 7The change...

Is the mattress important in helping babies keep warm?—Paradoxical effects of a sleeping surface with negligible thermal resistance

“…The values obtained were very similar to those previously reported for infants of similar ages (14,15,17,21).…”

“…1). This gave an overall predicted effective thermal resistance (taking account of body surface area covered) for clothing and sleeping bag of approximately 3.3 tog (excluding diaper), which from our previous studies (14–16) we calculated would provide a thermoneutral environment with a room temperature above 19–20°C. (The tog value of a fabric is defined as 10 times the temperature difference in degree centigrade between its two faces when the heat flow is equal to 1 W/m 2 ) (14).…”

Interleukin-6 and the serotonergic system of the medulla oblongata in the sudden infant death syndrome

“…It is also the site for several neurotransmitter abnormalities in SIDS, including in 5-HT, muscarinic, and kainate receptor binding [21, 32–34]. It is well documented that CO 2 levels are elevated during severe neonatal infection [2] and, interestingly, even mild upper respiratory infection may increase CO 2 levels in infants over 3 months of age [9]. Animal studies indicate that the CO 2 elevation can be attributed to a hyper-metabolic state induced by proinflammatory cytokines [15].…”

“…A major site of 5-HT cell bodies in the human infant brainstem is in the arcuate nucleus, the putative site for central carbon dioxide (CO 2 ) sensitivity in humans and animal models [10, 26, 30, 37]. In this regard, the synergistic effect of prone sleeping and infection on SIDS risk may be a “set-up” for CO 2 accumulation, as both rebreathing in the face-down (prone) position and increased metabolism due to infection may increase CO 2 levels [2, 9, 18, 51]. Death may be triggered if CO 2 -sensing regions in the brainstem, such as the arcuate nucleus, are compromised and cannot mount an arousal response to protect the infant from the dangerous situation.…”

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

“…A third alternate explanation of age of death in SIDS suggested by Fleming et al, 34 involves heat stress. They found that younger infants with upper respiratory infections rarely developed a fever, compared with infants older than 3 months, who also had higher metabolic rates even without a fever, thus subjecting the infants beyond one month of age to greater vulnerability to heat stress and SIDS.…”