Interactions between thermoregulation and the control of respiration in infants: possible relationship to sudden infant death

Fleming, Peter; Levine, M R; Azaz, Y; Wigfield, R; Stewart, Audrey

doi:10.1111/j.1651-2227.1993.tb12878.x

Cited by 81 publications

(41 citation statements)

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“…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 7 The change in metabolic rate over the first three months after birth, which, when expressed in terms of heat loss for each unit of surface area amounts to an increase of over 50%, might be expected to put infants aged 3 months at a higher risk of the adverse effects of a warm environment than younger infants.8 In the Avon study the risk of SIDS was increased by the presence of heavy wrapping only for those aged more than 70 days.…”

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

Fleming

Howell

Clements

et al. 1994

Archives of Disease in Childhood

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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...

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

Fleming

Howell

Clements

et al. 1994

Archives of Disease in Childhood

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“…22,24 Therefore, it has been suggested that thermal stress, with or without moderate increases in body temperature, can result in fatal disruption of vital systems among infants predisposed to SIDS. 1,25 It has been proposed that congenital or acquired anatomic abnormalities in brainstem centers regulating respiratory or cardiovascular stability could represent the underlying defects that render SIDS infants susceptible to death resulting from heat stress. 26 Our reasoning in assuming that a substantial number of infants at risk for SIDS experienced significant heat stress is as follows.…”

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confidence: 99%

Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study

2004

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ABSTRACT. Objectives. To determine the role of heat stress in sudden infant death syndrome (SIDS) by examining the SIDS rates during periods of extreme environmental temperatures in a period when most infants were placed prone for sleep.Design. A retrospective study of SIDS rates and mortality rates attributable to excessive environmental heat in relationship to climatologic temperature was performed. Data were collected for each of 454 counties in 4 states (Arkansas, Georgia, Kansas, and Missouri) from May 1 to September 30, 1980, and were then summed to yield the mortality rates for each 5°F (2.8°C) temperature range.Results. 2 analyses revealed significant relationships for heat-related mortality rates and both the maximal daily temperature and mean daily temperature but demonstrated no such relationships for SIDS rates. No association between SIDS rates and heat-related mortality rates was found with Spearman's ranked correlation, for either the maximal daily temperature or the mean daily temperature.Conclusions. On the basis of our findings of no significant association between SIDS and either measure of temperature during periods of high heat stress-related death rates, it seems unlikely that the heat stress associated with the combination of prone sleep positions and elevated environmental temperatures has a significant role in the development of SIDS. Pediatrics 2004; 113:e586 -e592. URL: http://www.pediatrics.org/cgi/ content/full/113/6/e586; SIDS, thermal stress, bedding, overwrapping, sleep position.ABBREVIATIONS. SIDS, sudden infant death syndrome; T max , maximal daily temperature; T avg , average daily temperature. T he thermal stress theory for sudden infant death syndrome (SIDS) states that many SIDS deaths occur as a result of increased demands on thermoregulatory mechanisms attributable to a prone sleep position, increased ambient temperature, and/or a decreased ability to eliminate body heat as a result of excessive clothing covering the infant. 1 Although the relationship between climatic temperature and SIDS incidence has been examined carefully, the studies were performed predominantly in nations without extreme temperature variations, such as Great Britain, Tasmania, and New Zealand. [2][3][4][5] Such research has consistently associated increased SIDS incidence with colder outdoor temperatures. It has been suggested that some parents may respond to such cold waves by overwrapping infants or excessively increasing room temperatures. 3 In contrast, a cross-cultural study found comparatively weak relationships between climatic temperature and SIDS incidence in communities in the United States. 6 Therefore, it is possible that seasonal overwrapping of infants may not be a major cause of SIDS in the United States.Sections of the United States, particularly the Midwest, are subject to periodic heat waves, which can lead to severe epidemics of deaths attributable to exposure to excessive heat. 7 Such conditions present an opportunity to examine the effect of increased environmental temperature o...

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“…The primary evidence for this comes from epidemiological studies. These studies have found increased environmental temperature and/or history of heavy sweating in association with some SIDS cases (6,26, 27). Despite this, the potential physiological mechanisms linking heat stress to SIDS are unclear.…”

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confidence: 97%

“…It has been suggested that thermal stress with or without actual increase in body temperature (T B ) may be causal in many SIDS cases (6,12). The primary evidence for this comes from epidemiological studies.…”

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Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS

Kahraman

Thach

2004

Journal of Applied Physiology

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Kahraman, Levent, and Bradley T. Thach. Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS. J Appl Physiol 97: 669 -674, 2004; 10.1152/japplphysiol.00895.2003.-The physiological mechanisms that might be involved in an association between heat stress and sudden infant death syndrome (SIDS) are obscure. We tested the hypothesis that a combination of acute hypoxia and elevated body temperature (TB) might prevent autoresuscitation from hypoxic apnea (AR). We exposed 21-day-old mice (total ϭ 216) to hyperthermia (40.5-43.5°C), hypoxia, or a combination of the two. Neither hyperthermia alone (40.5-42.5°C) nor hypoxia alone was found to be lethal, but the combination produced failure to AR during the first hypoxic exposure with increasing frequency as TB increased. The ability to withstand multiple hypoxic exposures was also reduced as T B increased. In contrast, heat stress causing moderate TB increase (40.5°C) had no effect on survival. Increased T B (43.5°C) reduced gasping duration and number of gasps. It increased heart rate during anoxia but did not alter gasping rate. Furthermore, the oxygenindependent increase in heart rate observed before gasping failure was usually delayed until after the last gasp in hyperthermic animals. Mild dehydration occurred during T B elevation, but this did not appear to be a primary factor in AR failure. We conclude that a thermal stress, which by itself is nonlethal, frequently prevents AR from hypoxic apnea. This may be due, at least in part, to decreased gasp number and duration as well as to hyperthermia-related asynchrony of reflexes regulating heart and gasping frequencies during attempted AR. hypoxic gasping; dehydration; hypoxic survival time; sudden infant death syndrome SUDDEN INFANT DEATH SYNDROME (SIDS) occurs in infants during a relatively brief period of development with peak incidence at 2-3 mo of age. It has been suggested that thermal stress with or without actual increase in body temperature (T B ) may be causal in many SIDS cases (6, 12). The primary evidence for this comes from epidemiological studies. These studies have found increased environmental temperature and/or history of heavy sweating in association with some SIDS cases (6,26, 27). Despite this, the potential physiological mechanisms linking heat stress to SIDS are unclear.Healthy infants have frequently been observed to autoresuscitate (AR) from prolonged apnea without apparent ill effects, indicating that this can be an important mechanism for surviving severe episodes of hypoxia (22,32). Failure to AR from hypoxic apnea by gasping is well documented in SIDS cases, and it has been proposed that such failure could be a critical SIDS causal mechanism (21, 25). Examination of terminal recordings of infants dying of SIDS reveals that hypoxic apnea is followed by gasping, and yet AR fails during the first attempt. In contrast, infants with other diagnoses often have repeated successful AR attempts immediately b...

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Interactions between thermoregulation and the control of respiration in infants: possible relationship to sudden infant death

Cited by 81 publications

References 13 publications

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

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

Heat Stress and Sudden Infant Death Syndrome Incidence: A United States Population Epidemiologic Study

Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS

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