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A sleep dependent mechanism lor infant death on sheepskins
Abstract
To determine whether rebreathing of expired air is a plausible lethal mechanism of sudden death in infants sleeping face down on sheepskins.
Case reports of infants who died on sheepskins combined with a controlled study of effects of their respiratory microenvironment at death.
Research laboratory.
Rabbits used experimentally to assist in simulation of an infant's respiratory microenvironment. Rabbits breathed into sheepskin through the airway of an infant mannequin.
None.
Rebreathing of expired air was documented by carbon dioxide analysis of airway gas. Arterial blood gas analysis showed hypoxemia, hypercarbia, and acidosis in all experimental rabbits but not in controls. Rebreathing expired air was lethal for three of four experimental rabbits.
Infants sleeping prone on a sheepskin, with their faces straight down, experience potentially lethal rebreathing of expired air. Avoidance of the prone position would markedly reduce the risk of rebreathing expired air. The pronounced decrease in sudden infant death syndrome in southern New Zealand that followed a campaign to eliminate prone sleeping may have been attributable to reduced fatal rebreathing, as deaths of infants sleeping face down on sheepskins were common before the campaign.
... There is evidence that asphyxia, secondary to rebreathing of expired air, might be causal in some or many SIDS deaths (Kemp et al. 1993, Kemp and Thach 1993, Waters et al. 1996b, Campbell et al. 1997, Kemp et al. 1998 Infants sleeping prone for the first time have a 14-19-fold increased risk for SIDS compared to regular prone-sleepers (Côté et al. 2000). Côté et al found that of 157 SIDS cases studied, 139 were found in the prone position. ...
... There is evidence that asphyxia, secondary to rebreathing of expired air, might be causal in some or many SIDS deaths (Kemp et al. 1993, Kemp and Thach 1993, Waters et al. 1996b, Campbell et al. 1997, Kemp et al. 1998 Infants sleeping prone for the first time have a 14-19-fold increased risk for SIDS compared to regular prone-sleepers (Côté et al. 2000). Côté et al found that of 157 SIDS cases studied, 139 were found in the prone position. ...
... There is evidence that asphyxia, secondary to rebreathing of expired air in the prone sleeping position, with hypercapnic hypoxic alterations in blood-gas profiles that mimic those induced by OSA, might be causal in some or many SIDS deaths (Kemp et al. 1993 (presumably in response to hypoxia and hypercapnia) and return to sleep (Waters et al. 1996b). An intact arousal response to initiate head movement is a vital protective mechanism. ...
... Bark from the ti tree has the consistency of the outer "paper" layer of birch bark, and when used in bedding is in the form of chips 1 to 3 cm in diameter. Unless specific information was lacking, bedding associated with infant deaths was arranged for laboratory study as it had been beneath the baby at the time of death, as described in previous publications (7)(8)(9). ...
... Except for the estimate of softness, the techniques for measuring physical properties have been described in detail elsewhere (6,7,16). All measurements were repeated five times for each item of bedding. ...
... This measurement reflects the bedding's propensity to retain an altered contour in response to the mass of the mannequin's head. R. The change in pressure needed to create flow of 0.2 L/s through the mannequin's nares was used to calculate the R imposed by the bedding (7,8,15). ...
Soft bedding has been shown in epidemiologic studies to increase the risk for sudden, unexpected death in prone-sleeping infants. We compared the physical properties of conventional bedding to bedding from two sources: 1) bedding that covered the airways of victims of sudden infant death syndrome (SIDS) lying prone and face down at the time of death; and, 2) bedding associated with increased risk for SIDS in case-control studies (i.e. bedding filled with ti tree bark). Using simple mechanical models and the head from an infant mannequin, we measured the resistance to airflow, malleability, and capacity to limit CO2 dispersal of the bedding. We also describe a technique for quantifying bedding softness. The resistance and malleability were similar for the conventional bedding, the ti tree bedding, and the bedding from SIDS deaths (analysis of variance, p = 0.85 and 0.16). The ti tree bedding and the other bedding from SIDS cases differed from conventional bedding in two physical properties. Both groups were softer (p < or = 0.005) and limited CO2 dispersal to a greater degree (p < or = 0.009). The finding that increased capacity to limit CO2 dispersal is a consistent property of the bedding covering the airways of these SIDS victims and of bedding shown to be an epidemiologic risk factor for SIDS supports rebreathing of expired air as a mechanism underlying the association of certain kinds of bedding with SIDS.
... The nasal reflex described herein potentially could produce apnea in awake infants who nasally breathe 8% CO 2 [1], or the deaths of rabbit [20] and human infants [20,30] who nasally rebreathe their expired air. However, since nasal application of CO 2 caused marked cardiorespiratory depression only in high concentrations in anesthetized rats (present study --albeit they have decreased upper respiratory reflexes under anesthesia [36]), this possibility must be considered with caution. ...
... The nasal reflex described herein potentially could produce apnea in awake infants who nasally breathe 8% CO 2 [1], or the deaths of rabbit [20] and human infants [20,30] who nasally rebreathe their expired air. However, since nasal application of CO 2 caused marked cardiorespiratory depression only in high concentrations in anesthetized rats (present study --albeit they have decreased upper respiratory reflexes under anesthesia [36]), this possibility must be considered with caution. ...
Stimulation of the upper respiratory tract with air-borne irritants can result in dramatic alterations of cardiorespiratory rhythms that include apnea, bradycardia and selective peripheral vasoconstriction. Since carbon dioxide can stimulate receptors in the nasal passages, we wanted to determine if this odorless gas can induce the same autonomic changes as air-borne irritants. Passing 100% carbon dioxide through the nasal passages of rats anesthetized with chloralose-urethane produced apnea, a vagally-mediated bradycardia and a sympathetically-mediated increase in mean arterial blood pressure. Application of atropine blocked the bradycardia without affecting respiratory or blood pressure changes, while injection of prazosin eliminated blood pressure responses but did not affect heart rate or apnea. There were no significant autonomic responses to nasal application of 10, 25 or 50% carbon dioxide. The responses were mediated through the trigeminal innervation of the nasal mucosa since they could be blocked when the anesthetic procaine was applied to the nasal cavity. We conclude that these cardiorespiratory responses are due to stimulation of trigeminal nociceptors located within the nasal mucosa.
... 3 Although the concentration of carbon dioxide (CO 2 ) in the atmosphere is .03% to .04%, the exhaled air of infants contains 4% to 5% CO 2 , 4 and it has been speculated that under certain conditions, such as sleeping face down on soft bedding, extensive CO 2 accumulation around the infant's face may result in rebreathing, asphyxia, and suffocation. 3,5,6 The possibility of CO 2 rebreathing has mainly been studied in experimental in vitro and animal models, 3,[5][6][7][8][9][10] whereas studies in infants are limited. [11][12][13] We have previously shown that a significant number of SIDS victims are found with their head covered by bedding and usually in the prone position. ...
... 3 Although the concentration of carbon dioxide (CO 2 ) in the atmosphere is .03% to .04%, the exhaled air of infants contains 4% to 5% CO 2 , 4 and it has been speculated that under certain conditions, such as sleeping face down on soft bedding, extensive CO 2 accumulation around the infant's face may result in rebreathing, asphyxia, and suffocation. 3,5,6 The possibility of CO 2 rebreathing has mainly been studied in experimental in vitro and animal models, 3,[5][6][7][8][9][10] whereas studies in infants are limited. [11][12][13] We have previously shown that a significant number of SIDS victims are found with their head covered by bedding and usually in the prone position. ...
To study the consequences of getting the head covered by bedding (fiber quilt) on carbon dioxide (CO2) accumulation around the face, behavior, and physiologic responses during prone and supine sleep in infants to add understanding to why victims of sudden infant death syndrome are often found under the bedding. METHPDOLOGY: Of 33 healthy term, usually nonprone sleeping infants, behavior and computerized polysomnography were successfully recorded for 30 during prone and supine sleep at 21/2 months and for 23 prone and 25 supine at 5 months.
For both ages and body positions, covering the head resulted in significant CO2 accumulation around the face, fewer apneas (3 to 10 seconds), shorter duration of apneas after sighs, higher heart and respiratory rates, and peripheral skin temperature. Differences were generally greater at 21/2 than at 5 months. While covered, the prone position was associated with higher CO2 levels close to the face, slightly higher transcutaneous PCO2, and higher heart rates and peripheral skin temperatures than the supine position. In the supine position 23% were able to remove the cover from the head at 21/2 and 60% at 5 months, whereas only 1 infant of 5 months managed to remove the cover when prone.
The observed responses are consistent with a potential for distress when the head is covered, particularly when placed prone. Probably most important with respect to sudden infant death syndrome is the infants' inability to remove the bedding from the head upon awakening from prone sleep.
... The rebreathing theory has been criticized because, although this degree of hypercarbia is biologically significant, it is un-likely to cause CO 2 narcosis or rapid death (19,30,38,43). Hypoxemia has been noted in animal models of rebreathing (4,24,25); however, there has been no direct measurement of environmental oxygen (O 2 ) in animal or human models. O 2 content of inspired air during rebreathing has been assumed to reciprocate CO 2 levels, such that inspired O 2 ϭ room air O 2 minus end-inspiration CO 2 (30); however, effects of factors such as the respiratory exchange ratio on CO 2 and O 2 are unknown (8). ...
... Rapidly advancing CNS hypoxia in infants, as in others, is associated with rapid onset of coma. Once coma occurs, an arousal-related change in head position is not possible and death would presumably eventually occur as in animal models of rebreathing (22,24,25). Therefore, the current findings further advance the concept that hypoxemia, rather than hypercarbia, may be the more important factor when death occurs in infants sleeping with their faces covered by soft porous bedding. ...
Some infants sleep facedown for long periods with no ill effects, whereas others become hypoxemic. Rebreathing of expired air has been determined by CO(2) measurement; however, O(2) levels under such conditions have not been determined. To evaluate this and other factors influencing inspired gas concentrations, we studied 21 healthy infants during natural sleep while facedown on soft bedding. We measured gas exchange with the environment and bedding, ventilatory response to rebreathing, and concentrations of inspired CO(2) and O(2). Two important factors influencing inspired gas concentrations were 1) a variable seal between bedding and infants' faces and 2) gas gradients in the bedding beneath the infants, with O(2)-poor and CO(2)-rich air nearest to the face, fresher air distal to the face, and larger tidal volumes being associated with fresher inspired air. Minute ventilation increased significantly while rebreathing because of an increase in tidal volume, not frequency. The measured drop in inspired O(2) was significantly greater than the accompanying rise in inspired CO(2). This appears to be due to effects of the respiratory exchange ratio and differential tissue solubilities of CO(2) and O(2) during unsteady conditions.
... The concentration of 7% CO2 and 8% O2 was used since this was found to induce similar physiological parameters (decreased arousals and decreased respiratory responses) and provide comparable blood gases, as seen in OSA infants Tinworth, 2003, 2005). Moreover, this level of gas exchange was based on the findings of mechanical models of rebreathing where inspired CO 2 levels were found to range from 5 to 10% (Kemp and Thach 1993;Campbell et al., 1997). The control group (n = 8) received an air mix via the nasal mask, with tap switching but always in air, for either 1 (n = 4) or 4 (n = 4) days in the same study environment. ...
Orexin neuropeptides (OxA and OxB) and their receptors (OX1R and OX2R) are involved in maintenance of sleep and wakefulness, and are regulated by various environmental stimuli. We studied piglets, in the early neonatal period, exposed to 48-min of intermittent hypercapnic hypoxia (IHH; 7% O2/8% CO2) alternating with air. Three groups of 13-14 day-old piglets with IHH exposure of 1-day (1D-IHH) (n=7), 2-days (2D-IHH) (n=7) and 4-days (4D-IHH) (n=8) were compared to controls (exposed only to air, n=8). Immunoreactivity of OxA and OxB was studied in the piglet hypothalamic regions of the dorsomedial hypothalamus (DMH), perifornical area (PeF) and lateral hypothalamic area (LH). Results showed that after 1D- and 2D-IHH, total OxA and OxB expression decreased by 20% (p≤0.005) and 40% (p<0.001), respectively. After 4D-IHH, the decrease in OxA and OxB was 50% (p<0.001). These findings indicate that a chronic IHH exposure induces greater changes in orexin neuropeptide expression than an acute 1-day exposure in the hypothalamus. This may be causally related to the dysregulation of sleep.
... Esta hipótesis se ha relacionado con la utilización de una cama blanda, con colchones de lana de oveja, o de pieles de animales, sobre los que el niño duerme boca abajo, lo cual facilita el que vuelve a inhalar el aire espirado (34)(35)(36) . Este tipo de colchones se utiliza generalmente en países fríos, a menudo sin calefacción central, por lo que los niños están a menudo muy arropados. ...
Introducción El síndrome de la muerte súbita infantil (MSI) conocido tam-bién como muerte en la cuna, consiste en la muerte de un niño, menor de un año de edad, en la que después de un estudio ne-crópsico completo, de una revisión detallada de su historia clí-nica y del examen del escenario y circunstancias de la muerte, no se encuentra ninguna causa que la justifique (1) . Su incidencia varía mucho entre distintos países. En Estados Unidos de América, se registra una tasa de 1,5-2 por mil naci-dos vivos y en Australia el 6,7 por mil. En la CE las diferen-cias también son llamativas y oscila entre el 0,1-0,3 por mil nacidos vivos de Italia, Portugal, Grecia o España y el 1,7-2,2 por mil de Irlanda, Francia y Reino Unido. En varios de estos países representa la primera causa de mortalidad infantil post-neonatal (2) . Estas variaciones en la incidencia se deben a la fal-ta de criterios unánimes en cuanto a la identificación de casos de MSI y a errores en los registros, pero también a diferencias reales entre unos países y otros que pueden depender de las dis-tintas prácticas de puericultura, hábitos y costumbres, en el ma-nejo del niño. Se conoce desde hace tiempo una serie de factores epide-miológicos de riesgo en relación con la MSI: bajo peso al nacer, madre soltera o muy joven, bajo nivel socioeconómico familiar, tabaquismo en el embarazo, muerte previa de un hermano por MSI, gemelaridad, etc. La identificación de factores de riesgo ha permitido adoptar medidas de protección sobre estos niños, como son los programas de monitorización continua en el do-micilio. Sin embargo, estos programas ejecutados en niños con riesgo no se han seguido, como era de esperar, de una dismi-nución de la tasa de muertes por MSI. Por otra parte, la capaci-dad de actuación para modificar estos factores de riesgo es muy limitada. En estos últimos años la investigación epidemiológica ha puesto de manifiesto otro tipo de factores de riesgo relaciona-dos de forma muy directa con el entorno del niño, con su medio ambiente y con los cuidados que se tienen con él, en los pri-meros meses. La importancia de conocer estas circunstancias del entorno del niño estriba en que son fácilmente modificables, por lo tanto, se puede actuar y disminuir el riesgo y la inciden-cia de la MSI. Esto es ya una realidad. La puesta en marcha de programas de información sobre determinados aspectos del cui-dado del niño se ha acompañado de una franca disminución de la tasa de mortalidad por MSI. Cambio de postura y disminución de la tasa de mortalidad por muerte súbita infantil en Navarra Resumen. La posición en decúbito prono durante el sueño ha sido referida como el factor de riesgo más importante en relación con la MSI. En nuestro país no se conocía la prevalencia del decúbito prono ni se había estudiado su relación con la MSI. En Navarra, según una encuesta efectuada sobre una muestra de 424 niños, nacidos entre el 1-2-92 y el 1-2-93, el 86,5% de los niños dormían en decúbito prono, el 5,6% en supino y el 3,5% sobre el costado. En el mes de marzo de 1993 se inició una campaña recomendando evitar el decúbito prono desde el nacimiento hasta el 6º mes. Después de la campaña, en una muestra de 441 niños, nacidos entre el 1-5-93 y el 1-5-94, solamente el 38,3% seguían durmiendo en prono, mientras que el 46% lo hacían en supino y el 9% sobre el costado. La tasa de mortalidad por MSI en Navarra en el período 1985-1993 fue de 1,3 por mil nacidos vivos, falleciendo una media de 6,3 niños/año. La tasa de mortalidad infantil después del cambio de postura en 1994 fue del 0,42 por mil nacidos vivos, con dos fallecimientos por MSI en dicho año. En Navarra, la disminución de la postura en prono se ha acompañado de forma significativa de una disminución de la tasa de mortalidad por MSI. An Esp Pediatr 1996;45:161-166. Palabras clave: Posición en decúbito prono; Muerte súbita infantil.
... 57 In this study, few infants were placed prone to sleep in either group, but the microenvironment could be similar to BS in terms of the warmer microenvironment and potential for rebreathing. 34,58 Increased arousals 21 may not be sufficient to protect the infant if the head is also covered by bedding. We have previously reported if the infant' s head is covered, the mother is involved in uncovering of the head ∼60% of the time, either initiating action herself or after prompting by the infant. ...
To identify desaturation events (arterial oxygen saturation [Sao(2)] <90%) and rebreathing events (inspired carbon dioxide (CO(2)) >3%), in bed-sharing (BS) versus cot-sleeping (CS) infants.
Forty healthy, term infants, aged 0 to 6 months who regularly bed-shared with at least 1 parent >5 hours per night and 40 age-matched CS infants were recruited. Overnight parent and infant behavior (via infrared video), Sao(2), inspired CO(2) around the infant's face, and body temperature were recorded during sleep at home.
Desaturation events were more common in BS infants (risk ratio = 2.17 [95% confidence interval: 1.75 to 2.69]), associated partly with the warmer microenvironment during BS. More than 70% of desaturations in both groups were preceded by central apnea of 5 to 10 seconds with no accompanying bradycardia, usually in active sleep. Apnea >15 seconds was rare (BS infants: 3 events; CS infants: 6 events), as was desaturation <80% (BS infants: 3 events; CS infants: 4 events). Eighty episodes of rebreathing were identified from 22 BS infants and 1 CS infant, almost all preceded by head covering. During rebreathing, Sao(2) was maintained at the baseline of 97.6%.
BS infants experienced more oxygen desaturations preceded by central apnea, partly related to the warmer microenvironment. Rebreathing occurred mainly during bed-sharing. Infants were at low risk of sudden infant death syndrome and maintained normal oxygenation. The effect of repeated exposure to oxygen desaturation in vulnerable infants is unknown as is the ability of vulnerable infants to respond effectively to rebreathing caused by head covering.
... SIDS can result from a deficit in autonomic control, in which cerebellar and vestibular structures fail to mount compensatory somatomotor and cardio-respiratory responses to a drop in blood pressure (Harper, 2001). During this time there is also an abrupt shift in the pattern of sleep-wake states with a marked decline in rapid eye movement (REM) sleep as well as an attenuation of ability to respond to hypoxia (Kemp & Thach, 1993;Trinder et al., 1990). In addition, circadian rhythms become more firmly established (Lodemore, Peterson, & Wailoo, 1992). ...
Human neonates spend the majority of their time sleeping. Despite the limited waking hours available for environmental exploration, the first few months of life are a time of rapid learning about the environment. The organization of neonate sleep differs qualitatively from adult sleep, and the unique characteristics of neonatal sleep may promote learning. Sleep contributes to infant learning in multiple ways. First, sleep facilitates neural maturation, thereby preparing infants to process and explore the environment in increasingly sophisticated ways. Second, sleep plays a role in memory consolidation of material presented while the infant was awake. Finally, emerging evidence indicates that infants process sensory stimuli and learn about contingencies in their environment even while asleep. As infants make the transition from reflexive to cortically mediated control, learned responses to physiological challenges during sleep may be critical adaptations to promote infant survival.
... Chiodini and Thach 5 found that, in a laboratory setting, prone-sleeping infants adopt the FSD position either spontaneously or in response to a noxious stimulus. In the FSD position, infants can rebreathe expired air, 6 especially when they are on soft bedding. 7 Infants in the FSD position are also at risk of upper airway obstruction; backward pressure on the mandible may lead to reduced oropharyngeal airway dimensions. ...
To determine the frequency and physiologic consequences of the face-straight-down (FSD) position, a postulated mechanism for the sudden infant death syndrome in prone-sleeping infants.
A survey of 151 infants, aged 1 to 7 months, in Montreal showed that 33% slept prone. Ten healthy prone-sleeping infants were studied in their homes at age 10 to 22 weeks. Infrared video and cardiorespiratory recordings were made on 3 consecutive nights in the prone (nights 1 and 3) and lateral (night 2) positions.
Infants maintained the prone position during 17 of 19 studies, but only 4 of 9 infants maintained the lateral position. The FSD position was observed 27 times in 17 prone nights: median frequency, 0.6 times per night (interquartile range, 0 to 4), and median total duration, 3.3 minutes (0.8% of total sleep time). A related position, the face-near-straight-down (FNSD) position, occurred more often, 5.3 (1 to 10) time per prone night, for 22.4 minutes (5.8% of total sleep time). Most periods in the FSD and FNSD position had no physiologic consequences; however, 14% of FSD and 3% of FNSD episodes were associated with airway obstruction as indicated by snoring, paradoxical respiratory movements, apnea, and/or increased partial pressure of transcutaneous carbon dioxide. Spontaneous arousal and head turning terminated the FSD and FNSD episodes.
The FSD and FNSD positions occur commonly in healthy prone-sleeping infants, and these positions can cause airway obstruction. We speculate that those infants with sudden infant death syndrome found in the FSD or FNSD position either have a congenital or an acquired defect in the arousal-head turning response or have encountered insurmountable environmental factors that prevent effective head turning.
... Thermal stress brought about by a contribution of infection, overwrapping, or excessive environmental heating has been shown to be associated with an increased risk of SIDS in a number of anecdotal reports (3-5, 9, 31, 32, 34, 37) and case-control studies (11,28,29); the issue is complex, inasmuch as thermal stress appears to be a risk factor exclusively in prone sleeping infants (11,28). Infants who sleep prone and in the face-straight-down position are at risk of rebreathing their expired air, resulting in significant asphyxia (7,23) and obstructive apnea from occlusion of the nares and/or from backward pressure on the mandible, which may lead to reduced oropharyngeal airway dimensions (36). Very little is known, however, about the possible consequences of hyperthermia (i.e., a ''forced'' increase in core temperature above the central nervous system thermoregulatory ''set point'' caused by overwrapping or excessive environmental heating) or fever (i.e., a ''regulated'' increase in core temperature that follows an increase in central nervous system thermoregulatory set point caused by pyrogens released during an infection) on baseline cardiorespiratory control or on protective responses that prevent hypoxia and death during rebreathing or apnea. ...
Failure to autoresuscitate by hypoxic gasping during prolonged sleep apnea has been suggested to play a role in sudden infant death. Furthermore, thermal stress brought about by a contribution of infection, overwrapping, or excessive environmental heating has been shown to be associated with an increased risk of sudden infant death, particularly in prone sleeping infants. The present experiments were carried out on newborn rat pups to investigate the influence of "forced" changes in core temperature on their time to last gasp during a single hypoxic exposure and on their ability to autoresuscitate during repeated exposure to hypoxia. On day 5 or 6 postpartum the pups were placed in a temperature-controlled chamber regulated to 33, 35, 37, 39, or 41 degrees C and exposed to a single period of hypoxia (97% N(2)-3% CO(2)) and their time to last gasp was determined, or they were exposed repeatedly to hypoxia and their ability to autoresuscitate from primary apnea was determined. Increases in core temperature brought about by changes in ambient temperature from 33 to 41 degrees C decreased the time to last gasp after a single hypoxic exposure and decreased the number of successful autoresuscitations after repeated hypoxic exposures. Thus our data support the hypothesis that forced changes in core temperature brought about by changes in ambient temperature influence protective responses in newborns that may prevent death during hypoxia, as may occur during single or repeated episodes of prolonged sleep apnea.
... [1][2][3][4][5][6][7][8][9] Proposed, but uncertain, mechanisms underlying this association include upper airway obstruction, rebreathing of expired air, thermal stress, reduced cerebral blood flow, and a higher arousal threshold. [10][11][12][13][14][15][16][17] However, no adverse eVects of the prone position on respiratory mechanics have been found in term infants, and, to the contrary, studies of preterm infants suggest that the prone position is physiologically advantageous. [18][19][20][21][22][23][24] Consequently, no specific posture induced compromise of respiratory mechanics has been linked with SIDS. ...
The physiological basis underlying the decline in the incidence of sudden infant death syndrome (SIDS) associated with changing the sleep position from prone to supine remains unknown.
To evaluate diaphragm thickness (t(di)) and shortening in healthy term infants in the prone and supine positions in order to determine whether changes in body position would affect diaphragm resting length and the degree of diaphragm shortening during inspiration.
In 16 healthy term infants, diaphragm thickness at the level of the zone of apposition on the right side was measured using ultrasonography. Heart rate (HR), breathing frequency (f), and transcutaneous oxyhaemoglobin saturation (SaO(2)) were recorded simultaneously during diaphragm imaging with the infants in the supine and prone positions during quiet sleep.
At end expiratory (EEV) and at end inspiratory lung volumes (EIV), t(di) increased significantly in the prone position. The change in t(di) during tidal breathing was also greater when the infant was prone. SaO(2), HR, and f were not significantly different at EEV and at EIV in both positions.
In healthy term infants, placed in the prone position, the diaphragm is significantly thicker and, therefore, shorter, both at EEV and EIV. Diaphragm shortening during tidal breathing is greater when the infant is prone. In the prone position, the decreased diaphragm resting length would impair diaphragm strength, and the additional diaphragm shortening during tidal breathing represents added work performed by the diaphragm. This may compromise an infant's capacity to respond to stressful situations when placed in the prone position and may contribute to the association of SIDS with prone position.
Carbon dioxide (CO2) rebreathing is a recognized hazard, particularly for infants. A new thermal rebreathing method and apparatus have been developed for measuring and comparing the degree to which various soft bedding materials perform with respect to this hazard. The new methodology simplifies the evaluation process and uses less costly equipment than the incumbent expensive and complex CO2 rebreathing model. Using warm air as a proxy for CO2, it relies on a highly sensitive differential thermometer to measure air temperature differences that correlate to the level of rebreathing. The apparatus is portable and requires neither the use of a gas analyzer nor a source of CO2. Test results comparing the two methods show strong correlation validating the new thermal concept. The availability of a simple CO2 rebreathing method and apparatus will promote quantitative evaluation of this hazard among a wider group of users, including infant product developers and manufacturers. Additional studies are suggested to further develop the thermal rebreathing model.
The measurement of biochemical parameters is primarily done in centralized laboratories, in intensive care units, and in the operating theatre with near‐patient point‐of‐care testing (POCT). The measurement of carbon dioxide (CO2) in blood as a part of the so‐called blood gas panel. POCT is a patient‐centred diagnostic test that is not performed in a centralized laboratory, but in the hospital immediately near the operating room or intensive care or in the ambulance. CO2 is a gaseous waste product of metabolism and physiologically very tightly controlled. The CO2 balance is maintained by a carbonate buffer system in blood. Clinical blood gas analysis systems can be grouped into devices for single analysis of a discrete blood sample and continuous monitoring devices. The measurement of CO2 in human breath – called capnometry – is common practice in respiratory gas monitoring in intensive caremedicine, emergency medicine, and anaesthesiology.
The American Academy of Pediatrics has recommended since 1992 that infants be placed to sleep on their backs to reduce the risk of sudden infant death syndrome (SIDS). Since that time, the frequency of prone sleeping has decreased from >70% to ~20% of US infants, and the SIDS rate has decreased by >40%. However, SIDS remains the highest cause of infant death beyond the neonatal period, and there are still several potentially modifiable risk factors. Although some of these factors have been known for many years (eg, maternal smoking), the importance of other hazards, such as soft bedding and covered airways, has been demonstrated only recently. The present statement is intended to review the evidence about prone sleeping and other risk factors and to make recommendations about strategies that may be effective for further reducing the risk of SIDS. This statement is intended to consolidate and supplant previous statements made by this Task Force.
In Industrieländern stellt der plötzliche Kindstod die häufigste Todesursache bei Kindern im ersten Lebensjahr dar. Ein bekannter Risikofaktor ist die Hyperthermie. Morphologische Hinweise auf eine Hyperthermie existieren nicht, sodass nur die Umstände der Entdeckung, z. B. hohe Umgebungstemperaturen, warme Kleidung oder Bedeckung, eine erhöhte Körpertemperatur oder starkes Schwitzen hinweisgebend sind. Es ist bekannt, dass bei Zellstress, einschließlich thermischer Einwirkungen auf den Körper, die Expression von Hitzeschockproteinen (Hsp) zunimmt. Es sollte untersucht werden, ob eine vermehrte Expression von Hsp70 als Hinweis auf eine prämortale Hyperthermie in plötzlichen Säuglingstodesfällen nachgewiesen werden kann. In 54 plötzlichen Säuglingstodesfällen wurde deshalb Nierengewebe auf eine Hsp70-Expression untersucht. Zum Vergleich wurden 29 Brand- bzw. Hitzetodesfälle herangezogen. Bei allen Säuglingstodesfällen war die Expression von Hsp70 negativ, im Gegensatz zur positiven Reaktion in allen Fällen der Vergleichsgruppe. Die fehlende Expression von Hsp70 in plötzlichen Kindstodfällen schließt eine einflussnehmende Hyperthermie nicht aus. Bedeutend scheint hierbei der Temperaturschwellenwert thermischer Einwirkungen, der eine Hsp-Expression induziert.
We carried out a nationwide case-control study, comparing 393 case patients with sudden infant death syndrome (SIDS) with 1592 control subjects, in order to examine sheepskin bedding as a risk factor. Sheepskin use was similar for case patients and control subjects (both, 42%; adjusted odds ratio [OR] = 1.28; 95% CI = 0.92, 1.79). Sheepskin use among the control subjects was associated with socioeconomic advantage. The relative risk for SIDS with sheepskin use was significantly increased in the infants placed prone to sleep (adjusted OR = 1.70; 95% CI = 1.08, 2.67), but not for infants placed in the supine or lateral position (adjusted OR = 0.82; 95% CI = 0.45, 1.48). An interaction between sheepskin use and bed sharing was also found. Sheepskin use was associated with a decreased risk of SIDS among infants sharing beds (adjusted OR = 0.61; 95% CI = 0.38, 0.99), but an increased risk among infants not bed sharing (adjusted OR = 2.25; 95% CI = 1.32, 3.86). We conclude that if an infant needs to be placed prone to sleep for medical reasons, a sheepskin should not be used as underbedding. However, for infants placed supine to sleep, sheepskins are not associated with an increased risk of SIDS. (J Pediatr 1998;133:701-4)
Rebreathing of expired air may be a lethal hazard for prone sleeping infants. This paper describes a mechanical model to simulate infant breathing, and examines the effects of bedding on exhaled air retention. Under simulated rebreathing conditions, the model allows the monitoring of raised carbon dioxide (CO2) inside an artificial lung–trachea system. Resulting levels of CO2 (although probably exaggerated in the mechanical model compared with an infant, due to the model’s fixed breathing rate and volume) suggest that common bedding materials vary widely in inherent rebreathing potential. In face down tests, maximum airway CO2 ranged from less than 5% on sheets and waterproof mattresses to over 25% on sheepskins, bean bag cushions, and some pillows and comforters. Concentrations of CO2 decreased with increasing head angle of the doll, away from the face down position. Recreations of 29 infant death scenes also showed large CO2 increases on some bedding materials, suggesting these infants could have died while rebreathing.
A prospective case-control study of sudden infant death syndrome (SIDS) in Norway, Denmark and Sweden between September 1,1992 and August 31,1995 comprised 244 cases and 869 matched controls. After the introduction of risk-intervention campaigns, the SIDS incidence decreased from 2. 3/1000 live births in Norway, 1. 6 in Denmark and 1. 0 in Sweden to 0. 6/1000 or fewer in all the Scandinavian countries in 1995. The decrease paralleled a decline in the prone sleeping position and there was an accompanying parallel fall in total postneonatal mortality in all three countries. Thus, the risk-reducing campaigns for SIDS have been successful not only in Norway and Denmark, starting from relatively high incidences, but also in Sweden, starting from a low incidence. During the study period, a gradual increase was observed for the effects of prone sleeping, smoking and bottle-feeding as risk factors for SIDS.
Background. Apparent life-threatening events have a diverse pathophysiology; some may be related to positional asphyxia.
Case report. We report on an infant who was found in his cot with his face pressed into a foam-rubber pad covering the bars of his cot, and his head wedged into a hollow between these bars. The infant was cyanotic, hypotonic and gasping. After resuscitation he started to breathe spontaneously, but was still acidotic on admission to hospital.
Discussion. This case report demonstrates the potential risks associated with the use of additional bedding materials in infants' cots. The use of these materials should be strongly discouraged.
This study was carried out to determine whether bedding used by infants, who are at either high or low risk for sudden infant death syndrome (SIDS), differs in physical properties favoring rebreathing of exhaled gases.
We compared softness and limitation of carbon dioxide dispersal by bedding, using a mechanical model. A questionnaire was used to describe sociodemographic risk factors and sleep practices; bedding was studied in homes with a model positioned where each infant was found sleeping that morning.
The groups differed with respect to five sociodemographic risk factors (p values all < or = 0.0001). In addition, infants at higher risk were more likely to have been placed to sleep prone (46%, p = 0.02) by parents who were less likely to be aware of the risk associated with the prone position (62% aware, p = 0.005). Infants at higher risk had softer bedding (p < 0.0001, 54.1+/-17.2 cm2 vs 33.7+/-7.7 cm2 in contact with model), which caused more limitation of carbon dioxide dispersal (p = 0.008; CO2 retained, 0.60%+/-0.15% vs 0.34%+/-0.05%).
A series of infants who are at high risk for SIDS because of sociodemographic factors more often sleep on bedding that has physical properties favoring rebreathing, and their parents are less often aware of the risk associated with prone sleeping.
Prone sleeping position, use of soft mattresses and head covering by bedclothes are known risk factors for sudden infant death syndrome (SIDS). Rebreathing carbon dioxide (CO(2) ) may be a possible mechanism or a confounding factor of SIDS.
To compare the aeration properties of a new concept of infant sleeping surface (Net) to three commercial mattresses advertised to improve aeration and to two standard infant mattresses.
Two experiments were performed: (I) A container (head box), filled with 7% CO(2) mixture, was opened to the mattress to allow gas mixture to passively diffuse outside and equilibrate with the surrounding room air. (II) Simulation of normal breathing of an infant, using a unidirectional reciprocal syringe, to determine CO(2) accumulation within the head box.
CO(2) concentrations in the head box were continuously measured until CO(2) levels fell below 1% or for 5 min (experiment I), or until CO(2) accumulation levels plateaued or for 6 min (experiment II).
The Net had a significantly faster rate of CO(2) elimination (88.5 ± 4.6 and 91.9 ± 0.9 sec, Net alone and when covered with a sheet, respectively) compared to 238.3 ± 14.2 sec to 387.8 ± 7.9 sec for the other mattresses (P < 0.001). Only the Net was able to prevent CO(2) accumulation with maximal CO(2) levels (0.56 ± 0.03% and 1.16 ± 0.05%; Net alone and when covered with a sheet, respectively) significantly lower than the range of 4.6-6.3% for the other mattresses (P < 0.001).
The new sleeping surface exhibited significantly better aeration properties in dispersing CO(2) and in preventing its accumulation.
The cause of sudden infant death syndrome (SIDS) is unknown. Many mechanisms have been postulated, although thermal stress, rebreathing of expired gases and infection/inflammation seem the most viable hypotheses for the causation of SIDS. Deaths from SIDS have reduced dramatically following the recommendation not to place infants to sleep prone. Epidemiological data have shown that prone sleeping position is more risky in winter, colder latitudes, higher altitudes, if the infant is unwell or has excessive bedding or clothing. This suggests prone sleeping position involves either directly or indirectly a thermal mechanism. SIDS caused by an infective/inflammatory mechanism might be associated with deaths occurring during the night. Rebreathing of expired gases, airway obstruction, long QT syndrome and other genetic conditions may explain a small number of sudden unexpected deaths in infancy.
We assessed the gas dispersal potential of bedding articles used by 14 infants diagnosed with sudden unexpected infant death at autopsy. Of these cases, eight exhibited FiCO(2) values greater than 10% within 2.5 min, six of which were found prone and two supine. The results demonstrated that these eight beddings had a high rebreathing potential if they covered the babies' faces. We did not, however, take into account in our model the large tissue stores of CO(2). As some bicarbonate pools will delay or suppress the increase of FiCO(2), the time-FiCO(2) graphs of this study are not true for living infants. This model, however, demonstrated the potential gas dispersal ability of bedding. The higher the FiCO(2) values, the more dangerous the situation for rebreathing infants. In addition, FiO(2) in the potential space around the model's face can be estimated mathematically using FiCO(2) values. The FiO(2) graph pattern for each bedding item corresponded roughly to the inverse of the FiCO(2) time course. The FiO(2) of the above eight cases decreased by 8.5% within 2.5 min. Recent studies using living infants placed prone to sleep reported that some babies exhibited larger decreases in FiO(2) than increases observed in FiCO(2). While the decrease of FiO(2) in our model is still theoretical, CO(2) accumulation and O(2) deprivation are closely related. If a striking O(2) deficiency occurs in a short period, babies can lose consciousness before an arousal response is evoked and all infants could be influenced by the poor gas dispersal of bedding; the main cause of sudden death in infancy would thus be asphyxia. When the bedding is soft, the potential for trapping CO(2) seems to be high; however, it is impossible to assess it by appearance alone. We sought to provide some objective indices for the assessment of respiratory compromise in relation to bedding using our model. When a baby is found unresponsive with his/her face covered with poor gas dispersal bedding, we should consider the possibility of asphyxia.
A questionnaire survey was conducted to assess the impact of the April 1992 American Academy of Pediatrics Task Force Statement, "Infant Positioning and SIDS," on the routine advice provided by pediatricians in Minnesota to families with newborn infants regarding sleep practices, including sleep position. There was a trend toward more discussion between all pediatric practice groups and families regarding infant sleep practices following the AAP Sleep Position Statement (P < 0.001-0.003). Prone sleep recommendations ranged from 9.2% for newborn infants to 21.4% for infants 6 months of age. Recommendations for the supine or lateral sleep positions predominated at all infant ages. Pediatricians in private practice were more likely to identify the AAP Statement as establishing a medicolegal standard (P < 0.05). We conclude that the 1992 AAP Statement has had a significant impact on the routine advice provided to families regarding infant sleep practices, including infant sleep position.
The etiology and prevention of sudden infant death syndrome (SIDS) are among the more frustrating topics in pediatrics. This article addresses several clinically relevant issues, including the relationships between apnea and SIDS, the nature of the "terminal event," effectiveness of home monitoring, the role of gastroesophageal reflux in apparent life-threatening events, and the association between the prone sleeping position and SIDS. This article is intended to provide the clinician with an awareness of the issues and the scientific basis needed to understand their contribution to SIDS.
Although accidental suffocation has been suggested as a cause of sudden infant death syndrome in infants who are found prone with their faces straight down, the occurrence and effects on breathing of this position in living infants are unknown. We studied prone sleeping infants to see whether they will sleep with their faces straight down; whether they can spontaneously change from this position; the way that thermal stimuli or bedding softness influences this change; and whether rebreathing or airway obstruction occurs. We studied 11 healthy infants, aged 0.2 to 6 months, while they slept on soft and on firm bedding. Most infants slept facedown spontaneously or when turned to this position. All could turn their heads readily but slept facedown for variable periods. All infants put their faces straight down more often after cold than after warm stimuli. Obstructive apnea occurred only once, but rebreathing occurred in all subjects. When the infants were in the facedown position, inspired carbon dioxide was three times greater on soft than on hard bedding. End-tidal carbon dioxide partial pressure rose in all subjects while they were in the facedown position; in one infant, high end-tidal carbon dioxide partial pressure and desaturation occurred without signs of arousal. We conclude that infants sleeping facedown may occasionally have significant asphyxia; this sleep position may have a role in some infant deaths diagnosed as sudden infant death syndrome.
As part of a 1-year study of sudden unexpected infant deaths in St. Louis, we performed both a specialized death scene investigation and, in selected cases, a physiologic reconstruction of the death scene with a rabbit model. Those cases in which the infant was found face down with nose and mouth covered by bedding were chosen for the physiologic testing; our goal was to assess the potential for lethal rebreathing of expired air. The physiologic studies reconstructed the infants' premortem ventilatory environment by using the head from an infant mannequin positioned on the actual bedding on which an infant had died and a rabbit breathing through the mannequin's nares. The specialized scene investigation was carried out in 31 of 32 deaths from sudden infant death syndrome, diagnosed by the usual methods. Of 31 infants, eight died with their faces downward and covered by bedding, and the bedding was obtained for further study in seven of eight cases. The bedding had low resistance to airflow (6.25 to 22.6 cm H2O/L per second), and caused considerable rebreathing that was lethal to the rabbits in five of seven cases. We conclude that items of bedding in common use are capable of causing lethal rebreathing by prone-sleeping infants whose nose and mouth become covered; suffocation by rebreathing was the probable mechanism of death in a substantial number of these deaths that had been attributed to sudden infant death syndrome.
The nasal cavities were examined in 56 cases of sudden infant death syndrome (SIDS) and 26 control cases and the following criteria were compared: inflammatory infiltration of the nasal mucosa (SIDS 59%--controls 65%; P = 0.577), diapedesis of inflammatory cells (SIDS 38%--controls 42%; P = 0.678), epithelial desquamation (SIDS 62%--controls 85%; P = 0.043); hyperemia (SIDS 66%--controls 65%; P = 0.951) and hypersecretion of the seromucous glands (SIDS 55%--controls 69%; P = 0.233). Only epithelial desquamation was found significantly more often in the controls than in SIDS cases, but these alterations are unspecific and are influenced by the postmortem interval. The intensity of rhinitis was not different between the SIDS and control groups. The frequency of rhinitis is therefore not specific for the sudden infant death syndrome, and seems to be merely a result of the high incidence of upper respiratory tract infections in this age group. We speculate, however, that infections of the nose in conjunction with other factors, such as prone position, covering of the head, hyperthermia, parental smoking and immaturity of the central nervous system, could play a role in the pathogenesis of the sudden infant death syndrome.
A total of 206 cases of sudden infant deaths examined at the Institute of Science and Forensic Medicine, Singapore, over a 5 year period (1989-93) were identified to assess the pattern of sudden death in this age group, which was subdivided into the neonatal and post-neonatal periods. A total of 34% (70) of infant deaths occurred in neonatal life and the remaining 66% (136) in the post-neonatal period; 90% of the neonatal deaths were natural, of which over half were due to congenital heart disease and complications of prematurity. Unnatural deaths in this period were uncommon, there being only seven such deaths. In the post-neonatal period, unnatural deaths constituted 25% of the total with trauma and aspiration heading the list. Natural deaths in the post-neonatal period are predominantly due to infections (34%) and a group of sudden natural deaths with minimal findings (31%). The latter group may arguably represent cases of Sudden Infant Death Syndrome (SIDS). The yearly incidence of this group in our study varied between 0.08 to 0.2 per 1000 live births, which is considerably lower than the incidence quoted for Western populations. The criteria for the classification and the impact of sudden infant deaths in Asian countries are discussed.
Physical and geometrical conditions influencing carbon dioxide (CO2) accumulation near the face of a sleeping infant positioned deep in a cot or pram (open cot shaft) or underneath bedding (closed cot shaft) were investigated. By means of mathematical and data-based simulation, and an experimental rebreathing model, both hypothetical (dry, exhaled air +20 degrees C) and more physiological conditions (heated, humidified exhaled air, room temperature +20 degrees C; with and without pooling of cold air within the shaft) were tested. With exhaled air at +20 degrees C, the CO2 concentration increased to about 10% within 5 min. The increase was faster the smaller the volume, and the smaller the opening of the cot shaft. When expiratory air was heated, the CO2 concentration increased with the same speed as when the shaft was closed, but to only 0.1-0.3% when the shaft was open. Pooling of cold air in the shaft increased CO2 accumulation 70-200 times the concentration in air (to <5.5%) when the shaft was open. Turbulence of the air outside the open shaft reduced the increase in CO2 concentration. The experiments imply that CO2 may accumulate around an infant's head when placed deep in a cot or pram with the bedding and walls creating a narrow, vertical, shaft-like tunnel to the surrounding air. Although the CO2 concentration may theoretically attain dangerous levels in such circumstances, a rapid equilibrium between the air within and outside the cot usually occurs due to convection of the expiratory air and turbulence from drafts, the infant's body movements and breathing. Such factors will largely eliminated any significant rebreathing with the exception of the extreme situation when expired air is contained within a closed space.
Investigations of infants dying unexpectedly have reported up to 28% being found completely under bedding. No detailed physiological studies looking at the possibilities of asphyxia in this situation are available. The aim was to determine the potential for asphyxia under different types and thicknesses of bedding. A mechanical model of a 3-month-old infant's respiratory system was used. Bedding was positioned over the head in a supine position, and inspired carbon dioxide recorded. With a fixed respiratory rate and tidal volume, carbon dioxide accumulation increased with increasing layers of blankets. Up to 8.3% inspired carbon dioxide was recorded with more than four layers of blankets. A cotton sheet between the face and blankets reduced the accumulation by half. An infant found dead under bedding may have been exposed to an asphyxial stress. Suffocation from rebreathing trapped, expired gases can be a cause of death in this situation.
Suffocation by bedclothes became a popular diagnosis in the 1940s but gradually became replaced with the diagnostic label of Sudden Infant Death Syndrome (SIDS). In 1991 a paper purported that, instead of SIDS, pillows filled with polystyrene beads had caused death by rebreathing suffocation; this conclusion was reached on the basis of experiments with anesthetized rabbits breathing through a doll's head that was placed face down on the pillow. Because of the anesthesia, rabbits could not change their face down position. The doll's nares could not collapse, which would have resulted in rapid death due to conventional suffocation. The rabbits required up to 3 hours or more to die of hypercarbia and hypoxia. Studies in normal infants revealed that they turned from the face-down position after only 2 minutes. (The only infant who retained CO2 soon died of a fatal neurologic disorder, with central hypoventilation). Using the rabbit/doll's head and mechanical models, a wide range of bedding was indicted, including cushions, sheepskins, pillows, comforters, foam mattresses, and even simple blankets and sheets as potentially causing fatal rebreathing. Except for the use of pillows in general, as well as mattresses filled with kapok and bark, there has been no epidemiologic support for these indictments.
To establish, with the use of live sedated piglets on a range of bedding surfaces, the possibility of asphyxia when an infant is breathing face down into infant bedding surfaces, and to compare the results with those obtained with a mechanical model.
Piglets underwent tracheotomy and were attached to a silicon rubber model head of a 3-month-old infant. This was placed face down on bedding surfaces, and respiratory and blood gas data were collected for a 60-minute period.
All bedding surfaces but one showed some rebreathing. This was to lower levels than with the mechanical model, but the ranking of the surfaces by level of rebreathing was similar. Two piglets died within the 1-hour experimental time.
It is confirmed that the data from a mechanical model of rebreathing on different bedding surfaces are matched by those derived from a piglet model that responds normally to asphyxia.
Twenty to 52% of sudden infant death syndrome (SIDS) victims are found dead with their noses and mouths turned into underlying bedding. Several items of bedding have been shown to increase the risk for SIDS in case-control studies or to be associated with many SIDS deaths in case series. These items of bedding are after limit CO2 dispersal more, and cause more rebreathing of exhaled gases than bedding infrequently associated with SIDS. Rebreathing of exhaled gases may explain some prone deaths, and avoiding rebreathing of these gases is one possible mechanism for the reduction in SIDS when infants avoid prone sleep. Results supporting these statements are reviewed and discussed.
Unlabelled:
After national intervention campaigns, considerable declines in incidence for both sudden infant death (SID) and prone position have been observed worldwide. In the following investigation. German data on postinterventional risk factor patterns are presented for the first time. We analysed data from a 2-year population-based case-control study on SID carried out in two German districts between 1993 and 1994. We confirmed Complete covering of the baby (OR = 44.9, 95%-CI 95, 291), prone sleeping position (OR = 11.7; 5.3, 26.2), heavy maternal smoking during pregnancy (OR = 8.5; 3.2, 33.2 for > ten cigarettes per day), nonbreastfeeding (OR = 7.7; 2.7, 22.3) and missing maternal professional training (OR = 7.6; 3.6, 16.2) as risk factors for cot death. After adjustment for other major risk factors in a logistic regression model, sleeping on cushions lost statistical significance, whereas all other major risk factors remained relevant.
Conclusions:
Despite intervention campaigns, complete covering of the baby, prone position and heavy maternal smoking are still major risk factors for cot death. Except for sleeping on cushions, all major epidemiological risk factors for cot death act independently. Despite encouraging success in the reduction of risk factors for cot death, there is still substantial need for future endeavours towards a further reduction of modifiable risk factors for SID.
A prospective case-control study of sudden infant death syndrome (SIDS) in Norway, Denmark and Sweden between September 1, 1992 and August 31, 1995 comprised 244 cases and 869 matched controls. After the introduction of risk-intervention campaigns, the SIDS incidence decreased from 2.3/1000 live births in Norway, 1.6 in Denmark and 1.0 in Sweden to 0.6/1000 or fewer in all the Scandinavian countries in 1995. The decrease paralleled a decline in the prone sleeping position and there was an accompanying parallel fall in total postneonatal mortality in all three countries. Thus, the risk-reducing campaigns for SIDS have been successful not only in Norway and Denmark, starting from relatively high incidences, but also in Sweden, starting from a low incidence. During the study period, a gradual increase was observed for the effects of prone sleeping, smoking and bottle-feeding as risk factors for SIDS.
Certain conditions in cases with pulmonary pathology such as thrombosis and embolism, pregnancy, asthma, drug abuse, Sudden Infant Death Syndrome (SIDS) and occupational exposures are particularly likely to come under critical scrutiny and may form the basis of allegations of medical negligence, wrongful death or product liability. Pathologists may play an important role in the resolution of these legal claims through the proper performance, interpretation and reporting of their examinations. Pathologists can also assist in the legal process by explaining pathologic findings and their significance, correlating them with the clinical course and addressing issues of causation.
We assessed some Japanese bedding on the assumption of the effects of air trapping using an infant mannequin. The change of CO2 concentration in the airway of a mannequin head placed on bedding was continuously monitored using a CO2 analyzer during simulated breathing. To compare the level of CO2 dispersal among different items of bedding, CO2 half time (t1/2) values were used. The t1/2 values were calculated by measuring the time required for the expired percent CO2 to reach 1/2 the initial percent end-tidal PCO2. We also measured softness and resistance to airflow (R) of the same items. As for the bedding, 4 types of futon and several types of bottom sheets/towels were combined. The t1/2 value in supine position was 9.8 seconds. When the model was placed prone on futon, the t1/2 values increased to 14.1 seconds (hard mattress type)--17.2 seconds (soft cotton-like futon). With respect to present Japanese baby futon (hard mattress type), there may be a relatively low potential for rebreathing to occur, compared with soft futon. In every case, the t1/2 value was prolonged by the use of a towel spread on the futon. CO2 dispersal may depend not only on the softness of the futon, but also on the combination of bottom sheet/towel and mattress. There was no relationship between R values and t1/2 values. The potential of rebreathing increased in face down position among all bedding, and supine position was the best CO2 dispersal position.
To examine whether the prone sleeping position may increase the risk for sudden infant death syndrome (SIDS), particularly in infants unused to prone sleep.
A 3-year (1987-1990) case-control study.
Nationwide study in New Zealand.
Four hundred eighty-five infants who died of SIDS and 1800 controls.
Infants were classified as unaccustomed to prone if their usual sleep position was nonprone and they were placed prone for the last sleep. Secondary prone was used to describe infants placed nonprone but found prone.
Infants usually and last placed nonprone were at the lowest risk for SIDS (odds ratio [OR], 1.0); those usually and last placed prone were at increased risk (adjusted OR, 4.6; 95% confidence interval, 3.4-6.3). Risk was greatly increased among infants unaccustomed to the prone position (adjusted OR, 19.3; 95% confidence interval, 8.2-44.8). These infants accounted for 8% (31/ 386) of all SIDS deaths. Ninety percent (28/ 31) of infants in this group were found prone, and 71% (20/28) of those found prone were found with their faces turned down into bedding-a position in which asphyxia has been implicated as a mechanism of death. In addition, 138 infants who died of SIDS were last placed nonprone. Forty-seven infants (34%) in this group were found prone (secondary prone), and 60% (28/47) of those found prone were found with their faces turned down into the bedding. This group accounted for 12% of all SIDS deaths. Most of these infants (91% [43/47]) were usually placed nonprone.
Infants placed supine to sleep were at the lowest risk of SIDS, which supports the recommendation that this is the preferred sleeping position for healthy infants. In New Zealand, 20% of SIDS deaths involved lack of experience with the prone sleeping position. Our findings suggest the possibility that an infant's competence in escaping from potentially lethal situations during prone sleep (eg, the face-down position) may be impaired by inexperience in prone sleeping. Great caution should be exercised in placing infants unaccustomed to the prone sleeping position in the prone position.
This article offers one institution's approach to implementation of the recommendations for infant sleep positioning as set forth by the American Academy of Pediatrics. The guidelines are directed toward healthy infants in the first year of life, a population not always encountered
by the neonatal nurse. The guidelines focus on supine sleep position and the minimization of additional bedding, both of which can be challenging when contrasted with accomplishing supportive positioning and the goals of developmentally supportive care for ill or preterm infants. A multidisciplinary
task force was formed to consider this challenge. The outcome is an evidence-based policy that is presented as an example for other clinicians. The policy addresses the following major components: sleep position with specific clinical exceptions, the use of bedding materials, play position
during awake states, and parent education with preparation for discharge. The article also outlines the process by which the task force plans to implement and evaluate necessary practice changes.
Experiments were carried out to determine if endogenous pyrogen-induced fever impairs protective responses of newborn rats to hypoxia. Twenty-seven 5- to 6-day-old conscious rat pups received a subcutaneous injection of 0.20 microg of recombinant rat interleukin-1beta (rrIL-1beta) per kilogram of body weight to induce fever, or an equal volume of vehicle. They were then either exposed to a single period of hypoxia produced by breathing an anoxic gas mixture (97 % N(2)-3 % CO(2)) and their time to last gasp was determined, or they were exposed repeatedly to hypoxia and their ability to autoresuscitate from primary apnoea was determined. Core temperature increased significantly following administration of rrIL-1beta but did not change following administration of vehicle (i.e. vehicle, 0.0 +/- 0.1 degrees C; rrIL-1beta, 0.7 +/- 0.3 degrees C; P < 0.001) before exposure to hypoxia. IL-1beta-induced fever did not alter the time to last gasp when the pups were exposed to a single period of hypoxia or the number of successful autoresuscitations upon repeated exposure to hypoxia. Thus, our data do not support the hypothesis that endogenous pyrogen-induced fever impairs the protective responses in newborns that may prevent death during hypoxia as may occur during single or repeated episodes of prolonged sleep apnoea.
Recent evidence suggests sudden infant death syndrome (SIDS) infants have a diminished capacity to respond to autonomic challenges during a vulnerable developmental period. We speculate that a dysfunction or altered trajectory in the development of the autonomic nervous system may be detected in utero and also may play a role in the pathogenesis of unexplained late stillbirth. Some fetuses, as well as infants, may be more vulnerable than others to autonomic challenges during periods of autonomic instability. Investigation of potential shared underlying mechanisms in both SIDS and unexplained stillbirth will require expanded epidemiological investigation of genetic and environmental correlates along with a systematic study of developmental physiology and neuropathology. As with SIDS, there are likely important interactions between genetic susceptibility and environmental exposures occurring during gestation, which lead to infants who have altered trajectories or deficits in autonomic function and who need to be identified before they enter the periods of greatest risk.
To establish the CO2 dispersion and retention properties of some mattresses and bed coverings commercially available in Australia.
Five mattresses were studied in (i) an in vivo model in which an infant's head was covered by a headbox, rebreathing was allowed to occur, and the final steady state CO2 concentration was measured; and (ii) an in vitro model in which 5% CO2 in a headbox was allowed to disperse, and the time taken for the concentration to reach 1% was measured. Five types of bedcover were studied in (i) an in vivo model in which an infant's head was covered by a bedcover and the final steady state CO2 concentration was measured; and (ii) an in vitro model in which 5% CO2 under a bedcover was allowed to disperse, and the time taken for the concentration to reach 1% was measured.
The steady state CO2 concentrations ranged from 0.6% to 3.0% for the mattresses (P < 0.05). The time for CO2 to disperse ranged from 5.5 min to 30.4 min (P < 0.05). Steady state CO2 concentrations ranged from 2.5% to 3.6% for the bedcoverings (P > 0.05). The time for CO2 to disperse ranged from 5.4 min to 7.7 min (P > 0.05).
Some commercial cot mattresses and bedcoverings allow high concentrations of CO2 to accumulate in rebreathing environments. Some mattress types studied were more diffusive to CO2, whereas there was no difference between the bedcovers studied. This may have implications for vulnerable infants at risk of sudden infant death syndrome.
The role of the N-methyl-D-aspartate (NMDA) receptor in cell death was evaluated in the piglet brainstem after exposure to intermittent hypercapnic hypoxia (IHH). Study groups comprised controls (n=6) and piglets exposed to IHH on 2 (n=6) or 4 (n=5) successive days prior to euthanasia. All piglets had the caudal medulla evaluated at 13-14 days of age using double immunohistochemistry for TUNEL and the NMDA receptor 1 (NR1) subunit. The percent of TUNEL positive neurons amongst NR1 (% TUN in NR1) and non-NR1 neurons (% TUN in non-NR1) was determined in eight nuclei. After 2 days of IHH, %TUN in NR1 was increased in the dorsal motor nucleus of the vagus (DMNV, P=0.007) and the inferior olivary nucleus (ION, P=0.05). After 2 days IHH, %TUN in non-NR1 neurons was increased in the lateral reticular nucleus (LRt, P=0.05), nucleus of the solitary tract (NTS, P=0.004) and gracile nucleus (P=0.05). After 4days IHH, the increase of %TUN in NR1 was sustained in the ION (P=0.05), while %TUN in non-NR1 neurons was sustained in NTS (P=0.04) and LRt (P=0.006). Daily IHH exposure induces neuronal death within NR1 and non-NR1 neurons, but the neuronal phenotype is consistent within affected brainstem nuclei. Involvement of the NMDA receptor tended to occur in nuclei with higher basal NR1 expression, and thus occurred in nuclei relevant to cardiorespiratory function. We speculate that IHH exposures, such as occurs during obstructive apnea or facial entrapment in prone sleeping during infancy, can induce abnormalities of cardiorespiratory control.
The effects of sleeping position upon body temperature were assessed by continuous monitoring of rectal temperature in 137 babies sleeping at home under conditions chosen by their parents. There were three groups of subjects: (1) normal babies aged 12-22 weeks whose temperature rhythms were developed, (2) normal babies aged 6-12 weeks who were developing their night time temperature rhythms, and (3) babies the night after diphtheria, pertussis, and tetanus immunisation, whose temperature rhythms were disturbed. Sleeping in the prone position was not associated with higher rectal temperatures at any time of night in young babies, nor did it exaggerate the disturbance of rectal temperature rhythm after immunisation. In older normal babies the prone position did not disturb rectal temperature in the first part of the night, though prone sleepers warmed a little faster prior to walking, especially in warm conditions. Prone sleepers were, however, born earlier in gestation and tended to be of lower birth weight. Normal babies can therefore thermoregulate effectively whatever their sleeping posture, even in warm conditions, though the prone position may make it slightly more difficult to lose heat. It is difficult to see how the prone position, even interacting with warm conditions, could induce lethal hyperthermia in otherwise normal babies. Perhaps the prone position is associated with other risk factors for sudden infant death syndrome.
A possible explanation for the cause of some cot deaths is examined by placing an appropriate cot death model on a cold wet sheet so that its "breath" is directed downwards across the sheet, thereby being cooled and becoming heavy enough to stay trapped in the hollow of the mattress. The breath is then available for rebreathing by the model. The level of carbon dioxide (CO2) "inhaled" is showed to be lower in nostril breathers, singletons and in bassinets and higher with mouth breathing models, in "twins", and in carry cots, especially if the model's head is accidentally covered. Under these conditions a living infant would become progressively acidotic due to inability to adequately excrete its metabolic CO2. This must inevitably be accompanied by increasing hypoxia. If left undisturbed in this predicament, it would rebreathe its own breath for the period of time between feeds and develop increasing degrees of asphyxia, depending on the circumstances outlined.