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Journal articles on the topic 'Sudden Infant Death Syndrome; Cot death'

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Published: 4 June 2021

Last updated: 9 February 2022

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1

Rambaud, Caroline, Cécile Cieuta, Danielle Canioni, Christine Rouzioux, Jean Lavaud, Philippe Hubert, Nicole Brousse, Michelle Rudler, and Gérard Chéron. "Cot death and myocarditis." Cardiology in the Young 2, no. 3 (July 1992): 266–71. http://dx.doi.org/10.1017/s1047951100001025.

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SummaryWe have investigated the hearts from 153 infants found dead in their cots at ages ranging from one month to one year. The deaths occurred over a period of five years (January 1986 to December 1990) and were studied in a center for the study of the sudden infant death syndrome located in Paris. The epidemiological characteristics of this group are:male predominance (sex ratio 1.43), age less than four months (82%), and a predominance of winter deaths. These are the characteristic features ofthe sudden infant death syndrome. Ofthe 143 children studied with the permission of their parents, 24 (16.8%–12 girls and 12 boys) had histological lesions consistentwith myocarditis according to the Dallas criteria. The histological diagnosis of myocarditis is based on the association of cellular necrosis with a mononuclear or mixed inflammatory infiltrate. Cytoplasmic vacuolization, the presence of inflammatory cells in myocytes, and rupture of the cell walls of myocardial fibres are the equivalent histological signs of cellular necrosis. Myocarditis was diversely associated with respiratory, hepatic, muscular, gastrointestinal and/or neurological involvement. Twelve infants had previously been ill. Two died during the course of a serious illness. In only four cases was a viral association demonstrated. This incidence of myocardial involvement, similar to thatdescribed elsewhere in the literature, suggests that myocarditis could be a pathogenic explanation of some deaths thought on general autopsy investigation to be sudden and unexplained.

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2

Howatson, A. G., W. J. A. Patrick, G. S. Fell, T. D. B. Lyon, A. A. M. Gibson, B. A. Richardson, E. A. Mitchell, et al. "Cot mattresses and sudden infant death syndrome." Lancet 345, no. 8956 (April 1995): 1044–46. http://dx.doi.org/10.1016/s0140-6736(95)90781-5.

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3

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Biovolatilization of antimony and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 4 (April 1998): 231–38. http://dx.doi.org/10.1177/096032719801700406.

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1 The aerobic filamentous fungus S. brevicaulis IMI 17297 methylated antimony from Sb2O3 substrate, with the formation of gaseous trimethylantimony (TMA). No evidence was found for the generation of other gaseous antimony compounds by this organism. 2 Biovolatilization of inorganic antimony was greatest during cultivation of the fungus on solid media at 258C, and occurred more readily from antimony (III) substrates than from antimony (V) substrates. 3 Under simulated cot environment conditions (CO2 enriched atmosphere, 338C) the fungus exhibited an altered morphology and a reduced capability to volatilize inorganic antimony from the pure compound. 4 No evidence of antimony biovolatilization from cot mattress PVC was found, unless antimony was released from PVC by heat treatment (at 80 or 1008C). 5 These data suggest that normal cot environment conditions are non-optimal for volatilization of antimony by S. brevicaulis, and that Sb2O3 in cot mattress PVC is not bioavailable. 6 Cot mattress isolates of S. brevicaulis also volatilized antimony (not encapsulated by PVC), whereas those of other filamentous fungi (Penicillium spp., Aspergillus niger, Aspergillus fumigatus, Alternaria sp.) and of bacteria (Bacillus spp.) did not. 7 The oxidation products of TMA may be the true determinants of toxicity for biogenic antimony gases produced in an aerobic environment.

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4

Richardson, B. A. "Cot mattresses and the sudden infant death syndrome." BMJ 310, no. 6986 (April 22, 1995): 1071. http://dx.doi.org/10.1136/bmj.310.6986.1071b.

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5

Mitchell, E. A., A. W. Stewart, and M. Clements. "Immunisation and the sudden infant death syndrome. New Zealand Cot Death Study Group." Archives of Disease in Childhood 73, no. 6 (December 1, 1995): 498–501. http://dx.doi.org/10.1136/adc.73.6.498.

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6

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Antimony leaching from cot mattresses and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 3 (March 1998): 138–39. http://dx.doi.org/10.1177/096032719801700302.

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1 Polyvinyl chloride (PVC) cot mattress covers from SIDS cases were investigated as potential sources of soluble (potentially ingestable) antimony in the cot environment. 2 Body fluids (urine, saliva) and proprietary domestic detergents/sterilizing fluids markedly enhanced leaching of antimony from PVC. Release of antimony was also enhanced at both low and high pH and by elevated temperature. The extent of antimony leaching did not correlate well with PVC content of this element. 3 These data do not support the assumption that postmortem analysis of antimony content proves exposure to gaseous antimony trihydride from mattress PVC. 4 Ingestion of antimony released from PVC could account for the high variability associated with reported detectable levels of antimony in liver from both SIDS and other infants. It could also explain suspected additional postnatal exposure to this element, which gives rise to elevated levels of Sb in the hair of some healthy infants.

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7

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Antimony leaching from cot mattresses and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 3 (March 1, 1998): 138–39. http://dx.doi.org/10.1191/096032798678908413.

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8

Tyler, J. W. "Sudden infant death and chronic infant disorders: The N.E.S.T. model versus the lethal Cot-death Syndrome hoax." Medical Hypotheses 30, no. 4 (December 1989): 271–75. http://dx.doi.org/10.1016/0306-9877(89)90036-4.

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9

Pisaniak, Paulina, Dominika Piękoś, Katarzyna Bąk, Patryk Stokłosa, and Dorota Ozga. "The battle with uneven opponent – Sudden Infant Death Syndrome." Pielegniarstwo XXI wieku / Nursing in the 21st Century 18, no. 2 (June 1, 2019): 132–35. http://dx.doi.org/10.2478/pielxxiw-2019-0013.

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AbstractSIDS is one of the biggest problems of modern medicine. In the diagnosis of SIDS, we take into account all possible diseases that may be the cause of death, as well as factors indicating an accident or murder. The etiology of SIDS is not yet known. There are several pathogenetic concepts, most of which refer to pathophysiological changes associated with nervous system hypoplasia. The most important risk factors include the effects of tobacco smoke, obstetric history, and incorrect sleep position. The role of risk factors in the pathogenesis of SIDS and their interdependence is still the subject of many studies. There are many theories developed on this subject, but none have been supported by scientific research and which is extremely difficult to carry out in this group of newborns. In most cases, medical help finds a newborn already dead, so it is difficult to say what is the main cause or marker of cot death. A considerable success in preventing the onset of sudden infant death syndrome turned out to be educational campaigns for parents - in order to follow up, an information leaflet was prepared with the basic recommendations in the prevention of SIDS. Among the parents of newborn children there are still many controversial opinions about risk factors in the onset of sudden infant death syndrome, the article contains and explains the meaning of individual activities that are considered to predispose to SIDS.

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10

Becroft, David M. O., John M. D. Thompson, and Edwin A. Mitchell. "Epidemiology of Intrathoracic Petechial Hemorrhages in Sudden Infant Death Syndrome." Pediatric and Developmental Pathology 1, no. 3 (May 1998): 200–209. http://dx.doi.org/10.1007/s100249900027.

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The possible effects of a wide range of sociodemographic and environmental factors on the incidence and distribution of petechiae were investigated in 485 sudden infant death syndrome (SIDS) cases from the New Zealand Cot Death Study. The number (nil, few, many) of macroscopic petechial hemorrhages in the visceral pleura, capsule of thymus, and epicardium was recorded in 458 of 474 autopsied SIDS cases. Other information was obtained from parental interview and obstetric records. Univariate analysis showed highly significant relationships ( P ≤ 0.005) between the frequency of petechiae at one or more sites and socioeconomic status, parity, breast feeding, age at death, time of death, sleep position, and head covering at death and lesser but significant relationships ( P ≤ 0.05) with Maori ethnicity, birth weight, gestation, pacifier use, and bed sharing. After multivariate analysis, significant associations remained between increased frequencies of thymic petechiae and parity (P = 0.0001), age at death (P = 0.0003), Maori ethnicity (P = 0.0019), pacifier use (P = 0.0001), and head covering at death (P = 0.0032); between increased frequencies of epicardial petechiae and head covering at death (P = 0.008) and an estimated time of death between 00:00 and 05:59 h ( P = 0.056); and between increased frequencies of pleural petechiae and maternal smoking ( P = 0.058) and parity ( P = 0.022). There was a decreased frequency of pleural petechiae in infants placed prone for their final sleep ( P = 0.058). The distribution and frequency of petechiae are affected by environmental factors, including known risk factors for SIDS, but these factors occur inconsistently across the three sites. The findings imply differences in the pathogenesis at each site but do not provide consistent support for previous theories of causation of petechiae.

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11

Scragg, R., E. A. Mitchell, B. J. Taylor, A. W. Stewart, R. P. Ford, J. M. Thompson, E. M. Allen, and D. M. Becroft. "Bed sharing, smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group." BMJ 307, no. 6915 (November 20, 1993): 1312–18. http://dx.doi.org/10.1136/bmj.307.6915.1312.

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12

STEWART, AJ, SM WILLIAMS, EA MITCHELL, BJ TAYLOR, RPK FORD, and EM ALLEN. "Antenatal and intrapartum factors associated with Sudden Infant Death Syndrome in the New Zealand Cot Death Study." Journal of Paediatrics and Child Health 31, no. 5 (October 1995): 473–78. http://dx.doi.org/10.1111/j.1440-1754.1995.tb00861.x.

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13

Becroft, David M. O., John M. D. Thompson, and Edwin A. Mitchell. "Pulmonary Interstitial Hemosiderin in Infancy: A Common Consequence of Normal Labor." Pediatric and Developmental Pathology 8, no. 4 (July 2005): 448–52. http://dx.doi.org/10.1007/s10024-005-0033-8.

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Deposits of hemosiderin are found frequently in the interstitium of the lungs of infants who die suddenly and have been a suggested marker for hypoxia during previous episodes of apnea. We studied the epidemiology of pulmonary interstitial hemosiderin (PIH) in 94 infants with a diagnosis of the sudden infant death syndrome that was established during the New Zealand Cot Death Study. Twenty-seven infants (29%) had widely distributed PIH. Associations were sought between PIH and variables on which information had been obtained from parental interviews or from medical records. Previous suggestions of associations with increasing birth weight and decreasing age at death were confirmed in multivariate analysis ( P = 0.0018 and P = 0.03, respectively) and with increasing gestation in univariate analysis ( P < 0.0001). PIH was not found in any of the 13 infants delivered by elective cesarean section compared with a 33% incidence in those exposed to labor ( P = 0.02). There was no association with previous apnea. We consider that the likely explanation of these findings is that PIH is a residue of interstitial hemorrhage caused by chest compression during labor that occurs particularly in larger infants of greater gestational age and then clears gradually during early infancy.

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14

Williams, S. M., B. J. Taylor, E. A. Mitchell, R. Scragg, R. P. Ford, and A. W. Stewart. "Sudden infant death syndrome in New Zealand: are risk scores useful? New Zealand National Cot Death Study Group." Journal of Epidemiology & Community Health 49, no. 1 (February 1, 1995): 94–101. http://dx.doi.org/10.1136/jech.49.1.94.

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15

Sherburn, R. E., and R. O. Jenkins. "Aerial release of bacteria from cot mattress materials and the sudden infant death syndrome." Journal of Applied Microbiology 98, no. 2 (February 2005): 293–98. http://dx.doi.org/10.1111/j.1365-2672.2004.02456.x.

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16

SHERBURN, R. "Cot mattresses as reservoirs of potentially harmful bacteria and the sudden infant death syndrome." FEMS Immunology and Medical Microbiology 42, no. 1 (September 2004): 76–84. http://dx.doi.org/10.1016/j.femsim.2004.06.011.

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17

Leditschke, J. Fred. "Surviving Childhood." Children Australia 14, no. 1-2 (1989): 25–27. http://dx.doi.org/10.1017/s0312897000002216.

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In the first month of life, prematurity and congenital anomalies account for the majority of deaths to children. Between one month and one year of age, the still unexplained Sudden Infant Death Syndrome (SIDS) or cot death remains very much an unsolved problem causing untold distress and grief to parents.If, however, we consider the childhood commencing at one month of age and carrying through until the completion of at least primary school and possibly secondary schooling, then accidents cause over a quarter of the deaths and, in considering those deaths in the first five years of life, drowning constitutes the number one cause. If we are looking at a spectrum from birth to fifteen years, deaths from motor vehicle accidents, whether as a passenger, pedestrian or bicyclist, are responsible for 50% of the deaths. Drowning features second on the list whilst such things as burns, poisoning, electrocution and suffocation now constitute a very small percentage of the deaths in childhood.

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18

Kelley, Joan, Dennis Allsopp, and David L. Hawksworth. "Sudden Infant Death Syndrome (SIDS) and the Toxic Gas Hypothesis: Microbiological Studies of Cot Mattresses." Human & Experimental Toxicology 11, no. 5 (September 1992): 347–55. http://dx.doi.org/10.1177/096032719201100508.

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1 Fifty infants' mattresses were studied to investigate the occurrence of viable fungal and bacterial propagules, with particular reference to Scopulariopsis brevicaulis which had been suggested to be implicated in SIDS cases. A total of 19 SIDS cases mattresses, 1 non-SIDS death, 20 used controls, and 10 new unused controls were examined. 2 Differences were found between SIDS and used controls in the variety of fungal species isolated and the numbers isolated from fillings; bacterial numbers were similar. 3 S. brevicaulis was isolated from only four mattresses, three of which were SIDS cases. It was not found in most of those on which death had occurred. 4 A number of potentially pathogenic or allergenic fungi, including Aspergillus fumigatus, were isolated more frequently from SIDS cases mattresses than new or used controls. 5 Scanning electron microscopy of mattress covers and fillings showed microbial 'biofilms' in the head areas of all SIDS cases examined. This was not seen on other samples. 6 The limited number of mattresses studied and the use of unmatched controls precludes the drawing of any general conclusions as to the significance of the biofilms or other fungi isolated. 7 Reports of the existence of a dimorphism in general growth forms of S. brevicaulis were investigated by growing and transferring authentic strains between a variety of growth media. 8 No 'slimy' state of this fungus was observed and dimorphism was not confirmed.

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19

Jenkins, R. O., and R. E. Sherburn. "Growth and survival of bacteria implicated in sudden infant death syndrome on cot mattress materials." Journal of Applied Microbiology 99, no. 3 (September 2005): 573–79. http://dx.doi.org/10.1111/j.1365-2672.2005.02620.x.

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20

WILSON, C. A., B. J. TAYLOR, R. M. LAING, S. M. WILLIAMS, and E. A. MITCHELL. "Clothing and bedding and its relevance to sudden infant death syndrome: Further results from the New Zealand Cot Death Study." Journal of Paediatrics and Child Health 30, no. 6 (December 1994): 506–12. http://dx.doi.org/10.1111/j.1440-1754.1994.tb00722.x.

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21

Saadi, A. T., C. C. Blackwell, M. W. Raza, V. S. James, J. Stewart, R. A. Elton, and D. M. Weir. "Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome." Epidemiology and Infection 110, no. 3 (June 1993): 507–17. http://dx.doi.org/10.1017/s0950268800050937.

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SUMMARYToxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSV). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from non-secretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa or anti-type-1 precursor significantly reduced bacterial binding (P < 0·01); however, attachment of the bacteria correlated only with the amount of Lewisa antigen detected on the cells (P < 0·01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context of factors previously associated with SIDS (mother's smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

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HOLGATE, S. T., C. WALTERS, A. F. WALLS, S. LAWRENCE, D. J. SHELL, S. VARIEND, P. J. FLEMING, P. J. BERRY, R. E. GILBERT, and C. ROBINSON. "The anaphylaxis hypothesis of sudden infant death syndrome (SIDS): mast cell degranulation in cot death revealed by elevated concentrations of tryptase in serum." Clinical & Experimental Allergy 24, no. 12 (December 1994): 1115–22. http://dx.doi.org/10.1111/j.1365-2222.1994.tb03316.x.

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23

Patel, Aloka L., Kathy Harris, and Bradley T. Thach. "Inspired CO2 and O2 in sleeping infants rebreathing from bedding: relevance for sudden infant death syndrome." Journal of Applied Physiology 91, no. 6 (December 1, 2001): 2537–45. http://dx.doi.org/10.1152/jappl.2001.91.6.2537.

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Some infants sleep facedown for long periods with no ill effects, whereas others become hypoxemic. Rebreathing of expired air has been determined by CO2 measurement; however, O2 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 CO2 and O2. 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 O2-poor and CO2-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 O2 was significantly greater than the accompanying rise in inspired CO2. This appears to be due to effects of the respiratory exchange ratio and differential tissue solubilities of CO2and O2 during unsteady conditions.

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Curran, Aidan K., Robert A. Darnall, James J. Filiano, Aihua Li, and Eugene E. Nattie. "Muscimol dialysis in the rostral ventral medulla reduced the CO2 response in awake and sleeping piglets." Journal of Applied Physiology 90, no. 3 (March 1, 2001): 971–80. http://dx.doi.org/10.1152/jappl.2001.90.3.971.

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Some victims of sudden infant death syndrome have arcuate nucleus abnormalities. The arcuate nucleus may be homologous with ventral medullary structures in the cat known to be involved in the control of breathing and the response to systemic hypercapnia. We refer to putative arcuate homologues in the piglet collectively as the rostral ventral medulla (RVM). We inhibited the RVM in awake and sleeping, chronically instrumented piglets by microdialysis of the GABAA receptor agonist muscimol. Muscimol dialysis (10 and 40 mM) had no effect on eupnea but caused a significant reduction in the response to hypercapnia during both wakefulness (34.8 ± 8.7 and 30.7 ± 10.1%, respectively) and sleep (36.7 ± 6.7 and 49.5 ± 8.9%, respectively). The effect of muscimol on the CO2 response was entirely via a reduction in tidal volume and appeared to be greater during non-rapid-eye-movement sleep. We conclude that the piglet RVM contains neurons of importance in the response to systemic CO2 during both wakefulness and non-rapid-eye-movement sleep. We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia, particularly during sleep, which could potentially be involved in the pathogenesis of sudden infant death syndrome.

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25

Blair, P. S., P. J. Fleming, I. J. Smith, M. W. Platt, J. Young, P. Nadin, P. J. Berry, J. Golding, the CESDI SUDI research group, and E. Mitchell. "Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome Commentary: Cot death---the story so far." BMJ 319, no. 7223 (December 4, 1999): 1457–62. http://dx.doi.org/10.1136/bmj.319.7223.1457.

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26

Jenkins, R. O., T.-A. Morris, P. J. Craig, W. Goessler, N. Ostah, and K. M. Wills. "Evaluation of cot mattress inner foam as a potential site for microbial generation of toxic gases." Human & Experimental Toxicology 19, no. 12 (December 2000): 693–702. http://dx.doi.org/10.1191/096032700670028460.

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Recent reports of biovolatilisation of phosphorus and antimony by anaerobic bacteria and of leaching of phosphorus and antimony fire-retardant additives from PVC cot mattress covers, indicate that the polyurethane inner-foam of cot mattresses could be a site for generation of toxic gases of group 15 elements. A toxic gas hypothesis for sudden infant death syndrome (SIDS) involving polyurethane foam of cot mattresses was proposed and tested experimentally. Levels of antimony, phosphorus, arsenic and bismuth were determined at four sites for 44 SIDS and 50 control (no death) cot mattress foams. There was no evidence to suggest that the levels of these elements in cot mattress foam have a causal relation to SIDS. Leaching of antimony trioxide from PVC mattress covers could account for detectable levels of this element in 52% of the cot mattress samples analysed. Volatile forms of antimony, phosphorus, arsenic and bismuth was not detected in the headspace of mixed or monoseptic cultures of anaerobic bacteria containing polyurethane foam. Past microbial activity had given rise to involatile methylated species of antimony in some of the cot mattress foams tested (61%, n = 24). Abiotic oxidation of biogenic trimethylatimony together with physical adsorption of methylantmony forms to the polyurethane foam matrix could account for the apparent absence of “escaped” volatile antimony species in culture headspaces of incubation vial. There was no evidence to suggest that levels of trimethylantimony or total methylantimony forms in cot mattress foams have a causal relation to SIDS.

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27

Miller, Marvin E., John G. Brooks, Nicholas Forbes, and Richard Insel. "Frequency of Medium-Chain Acyl-CoA Dehydrogenase Deficiency G-985 Mutation in Sudden Infant Death Syndrome." Pediatric Research 31, no. 4 (April 1992): 305–7. http://dx.doi.org/10.1203/00006450-199204000-00001.

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Carolan, Patrick L., James S. Kemp, James Ross, and William B. Wheeler. "Effect on CO2 Dispersal Rate of Commercial Products Marketed to Reduce Sudden Infant Death Syndrome Risk." Pediatric Research 45, no. 4, Part 2 of 2 (April 1999): 350A. http://dx.doi.org/10.1203/00006450-199904020-02083.

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29

Kaku, Noriyuki, Kenji Ihara, Yuichiro Hirata, Kenji Yamada, Sooyoung Lee, Hikaru Kanemasa, Yoshitomo Motomura, et al. "Diagnostic potential of stored dried blood spots for inborn errors of metabolism: a metabolic autopsy of medium-chain acyl-CoA dehydrogenase deficiency." Journal of Clinical Pathology 71, no. 10 (May 2, 2018): 885–89. http://dx.doi.org/10.1136/jclinpath-2017-204962.

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AimIt is estimated that 1–5% of sudden infant death syndrome (SIDS) cases might be caused by undiagnosed inborn errors of metabolism (IEMs); however, the postmortem identification of IEMs remains difficult. This study aimed to evaluate the usefulness of dried blood spots (DBSs) stored after newborn screening tests as a metabolic autopsy to determine the causes of death in infants and children who died suddenly and unexpectedly.MethodsInfants or toddlers who had suddenly died without a definite diagnosis between July 2008 and December 2012 at Kyushu University Hospital in Japan were enrolled in this study. Their Guthrie cards, which had been stored for several years at 4–8°C, were used for an acylcarnitine analysis by tandem mass spectrometry to identify inborn errors of metabolism.ResultsFifteen infants and children who died at less than 2 years of age and for whom the cause of death was unknown were enrolled for the study. After correcting the C0 and C8 values assuming the hydrolysation of acylcarnitine in the stored DBSs, the corrected C8 value of one case just exceeded the cut-off level for medium-chain acyl-CoA dehydrogenase (MCAD) deficiency screening. Genetic and biochemical analyses confirmed this patient to have MCAD deficiency.ConclusionDBSs stored after newborn screening tests are a promising tool for metabolic autopsy. The appropriate compensation of acylcarnitine data and subsequent genetic and biochemical analyses are essential for the postmortem diagnosis of inborn errors of metabolism.

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Young, Jacob O., Aron Geurts, Matthew R. Hodges, and Kevin J. Cummings. "Active sleep unmasks apnea and delayed arousal in infant rat pups lacking central serotonin." Journal of Applied Physiology 123, no. 4 (October 1, 2017): 825–34. http://dx.doi.org/10.1152/japplphysiol.00439.2017.

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Sudden infant death syndrome (SIDS), occurring during sleep periods, is highly associated with abnormalities within serotonin (5-HT) neurons, including reduced 5-HT. There is evidence that future SIDS cases experience more apnea and have abnormal arousal from sleep. In rodents, a loss of 5-HT neurons is associated with apnea in early life and, in adulthood, delayed arousal. As the activity of 5-HT neurons changes with vigilance state, we hypothesized that the degree of apnea and delayed arousal displayed by rat pups specifically lacking central 5-HT varies with state. Two-week-old tryptophan hydroxylase 2-deficient ( TPH2−/−) and wild-type (WT) rat pups were placed in plethysmographic chambers supplied with room air. At the onset of active (AS) or quiet (QS) sleep, separate groups of rats were exposed to hypercapnia (5% CO2) or mild hypoxia (~17% O2) or maintained in room air. Upon arousal, rats received room air. Apnea indexes and latencies to spontaneous arousal from AS and QS were determined for pups exposed only to room air. Arousal latencies were also calculated for TPH2−/− and WT pups exposed to hypoxia or hypercapnia. Compared with WT, TPH2−/− pups hypoventilated in all states but were profoundly more apneic solely in AS. TPH2−/− pups had delayed arousal in response to increasing CO2, and AS selectively delayed the arousal of TPH2−/− pups, irrespective of the gas they breathed. Thus infants who are deficient in CNS 5-HT may be at increased risk for SIDS in AS because of increased apnea and delayed arousal compared with QS. NEW & NOTEWORTHY Sudden infant death syndrome (SIDS) occurs during sleep and is associated with central serotonin (5-HT) deficiency. We report that rat pups deficient in central 5-HT ( TPH2−/−) are profoundly more apneic in active sleep (AS) but not quiet sleep (QS). Unlike control pups, the arousal of TPH2−/− pups in air, CO2, and hypoxia was delayed in AS compared with QS. Thus for infants deficient in central 5-HT, the risk of SIDS may be higher in AS than in QS.

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31

Itzhak, Nadav, and David Greenblatt. "Aerodynamic factors affecting rebreathing in infants." Journal of Applied Physiology 126, no. 4 (April 1, 2019): 952–64. http://dx.doi.org/10.1152/japplphysiol.00784.2018.

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The rebreathing of expire air, with high carbon dioxide and low oxygen concentrations, has long been implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants are placed to sleep in a prone (facedown) position. This study elucidates the effect of the aerodynamic parameters Reynolds number, Strouhal number, and Froude number on the percentage of expired air that is reinspired (rebreathed). A nasal module was designed that served as a simplified geometric representation of infant nostrils and placed above a hard, flat surface. Quantitative and flow visualization experiments were performed to measure rebreathing, using water as the working medium, under conditions of dynamic similarity. Different anatomic (e.g., tidal volume, nostril diameter), physiological (e.g., breathing frequency), and environmental (e.g., temperature, distance from the surface) factors were considered. Increases in Strouhal number (simultaneously faster and shallower breathing) always produced higher rebreathed percentages, because rolled-up vortices in the vicinity of the nostrils had less time to move away by self-induction. Positively and negatively buoyant flows resulted in significant rebreathing. In the latter case, consistent with a warm environment and a high percentage of rebreathed CO2, denser gas pooled in the vicinity of the nostrils. Reynolds numbers below 200 also dramatically increased rebreathing because the expired gas pooled much closer to the nostrils. These results clearly elucidated how the prone position dramatically increases rebreathing by a number of different mechanisms. Furthermore, the results offer plausible explanations of why a high-temperature environment and low birthweight are SIDS risk factors. NEW & NOTEWORTHY A fundamentally new aerodynamics-based approach to the study of rebreathing of expired air in infants is presented. Rebreathing is implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants sleep in a prone position. This is the first time that aerodynamic parameters are systematically varied and their effects on rebreathing quantified. The study provides us with a deeper understanding of the effects of breathing frequency, tidal volume (birthweight) and environmental conditions.

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Cushing, J. M. "Book Reviews : Cot Deaths, Coping with Sudden Infant Death Syndrome by Jacquelynn Luben. Published by Thorsons Publishing, 1986. Price: £5.99. Paperback. Pp 191. ISBN: 0 7225 1255 4." Journal of the Royal Society of Health 107, no. 4 (August 1987): 159. http://dx.doi.org/10.1177/146642408710700418.

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Penatti, E. M., A. V. Berniker, B. Kereshi, C. Cafaro, M. L. Kelly, M. M. Niblock, H. G. Gao, H. C. Kinney, A. Li, and E. E. Nattie. "Ventilatory response to hypercapnia and hypoxia after extensive lesion of medullary serotonergic neurons in newborn conscious piglets." Journal of Applied Physiology 101, no. 4 (October 2006): 1177–88. http://dx.doi.org/10.1152/japplphysiol.00376.2006.

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Acute inhibition of serotonergic (5-HT) neurons in the medullary raphé (MR) using a 5-HT1A receptor agonist had an age-dependent impact on the “CO2 response” of piglets ( 33 ). Our present study explored the effect of chronic 5-HT neuron lesions in the MR and extra-raphé on the ventilatory response to hypercapnia and hypoxia in piglets, with possible implications on the role of 5-HT in the sudden infant death syndrome. We established four experimental groups. Group 1 ( n = 11) did not undergo any treatment. Groups 2, 3, and 4 were injected with either vehicle or the neurotoxin 5,7-dihydroxytryptamine in the cisterna magna during the first week of life ( group 2, n = 9; group 4, n = 11) or second week of life ( group 3, n = 10). Ventilation was recorded in response to 5% CO2 (all groups) and 12% O2 ( group 2) during wakefulness and sleep up to postnatal day 25. Surprisingly, the piglets did not reveal changes in their CO2 sensitivity during early postnatal development. Overall, considerable lesions of 5-HT neurons (up to 65% decrease) in the MR and extra-raphé had no impact on the CO2 response, regardless of injection time. Postlesion raphé plasticity could explain why we observed no effect. 5,7-Dihydroxytryptamine-treated males, however, did present a lower CO2 response during sleep. Hypoxia significantly altered the frequency during sleep in lesioned piglets. Further studies are necessary to elucidate the role of plasticity, sex, and 5-HT abnormalities in sudden infant death syndrome.

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Highet, Amanda R., Anne M. Berry, Karl A. Bettelheim, and Paul N. Goldwater. "The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants." Journal of Medical Microbiology 58, no. 3 (March 1, 2009): 285–89. http://dx.doi.org/10.1099/jmm.0.005322-0.

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Consistent pathological findings in sudden infant death syndrome (SIDS) are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. A key candidate infectious agent that is possibly involved is Escherichia coli, given its universal early colonization of the intestinal tract of infants and an increased frequency of toxigenic and mouse-lethal isolates from SIDS compared with comparison infants. An explanation for these findings has yet to be identified. Using PCR, we screened E. coli isolates from 145 SIDS and 101 dead control and healthy infants for three new candidate pathogenicity-related genes: clyA (cytolysin A), irp2 [high-pathogenicity island (HPI)-specific gene] and cdt (cytolethal distending toxin). The results failed to show a positive correlation with SIDS, instead proving that clyA and irp2 genes were common to the infant intestinal E. coli. Interestingly we observed a high rate of carriage of these two potentially pathogenic genes in E. coli from healthy infants in the absence of diarrhoeal disease, and we report that in a number of cases, the detection of HPI-specific genes was predictable by serotype. Despite the lack of associations defined so far, there remains the likelihood that genetic determinants influence the interactions between E. coli and the host, so these factors may be part of the multi-factorial aspect of SIDS.

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Messier, Michelle L., Aihua Li, and Eugene E. Nattie. "Inhibition of medullary raphé serotonergic neurons has age-dependent effects on the CO2 response in newborn piglets." Journal of Applied Physiology 96, no. 5 (May 2004): 1909–19. http://dx.doi.org/10.1152/japplphysiol.00805.2003.

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Medullary raphé serotonergic neurons are chemosensitive in culture and are situated adjacent to blood vessels in the brain stem. Selective lesioning of serotonergic raphé neurons decreases the ventilatory response to systemic CO2 in awake and sleeping adult rats. Abnormalities in the medullary serotonergic system, including the raphé, have been implicated in the sudden infant death syndrome ( 48 ). In this study, we ask whether serotonergic neurons in the medullary raphé and extra-raphé regions are involved in the CO2 response in unanesthetized newborn piglets, 3-16 days old. Whole body plethysmography was used to examine the ventilatory response to 5% CO2 before and during focal inhibition of serotonergic neurons by 8-hydroxy-2-di- n-propylaminotetralin (8-OH-DPAT), a 5-HT1A receptor agonist. 8-OH-DPAT (10 or 30 mM in artificial cerebrospinal fluid) decreased the CO2 response in wakefulness in an age-dependent manner, as revealed by a linear regression analysis that showed a significant negative correlation ( P < 0.001) between the percent change in the CO2 response and piglet age. Younger piglets showed an exaggerated CO2 response. Control dialysis with artificial cerebrospinal fluid had no significant effect on the CO2 response. Additionally, 8-OH-DPAT increased blood pressure and decreased heart rate independent of age ( P < 0.05). Finally, sleep cycling was disrupted by 8-OH-DPAT, such that piglets were awake more and asleep less ( P < 0.05). Because of the fragmentary sleep data, it was not possible to examine the CO2 response in sleep. Inhibition of serotonergic medullary raphé and extra-raphé neurons decreases ventilatory CO2 sensitivity and alters cardiovascular variables and sleep cycling, which may contribute to the sudden infant death syndrome.

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36

Sudhan, Lavanya, Leonardi, Neri, and Sekar. "Monitoring of Chemical Risk Factors for Sudden Infant Death Syndrome (SIDS) by Hydroxyapatite-Graphene-MWCNT Composite-Based Sensors." Sensors 19, no. 15 (August 5, 2019): 3437. http://dx.doi.org/10.3390/s19153437.

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Sensing properties of chemical sensors based on ternary hydroxyapatite-graphene-multiwalled carbon nanotube (HA-GN-MWCNT) nanocomposite in the detection of chemical substances representing risk factors for sudden infant death syndrome (SIDS), have been evaluated. Characterization data of the synthesized composite have shown that the graphene-MWCNT network serves as a matrix to uniformly disperse the hydroxyapatite nanoparticles and provide suitable electrical properties required for developing novel electrochemical and conductometric sensors. A HA-GN-MWCNT composite-modified glassy carbon electrode (HA-GN-MWCNT/GCE) has been fabricated and tested for the simultaneous monitoring of nicotine and caffeine by cyclic voltammetry (CV) and square wave voltammetry (SWV), whereas a HA-GN-MWCNT conductive gas sensor has been tested for the detection of CO2 in ambient air. Reported results suggest that the synergic combination of the chemical properties of HA and electrical/electrochemical characteristics of the mixed graphene-MWCNT network play a prominent role in enhancing the electrochemical and gas sensing behavior of the ternary HA-GN-MWCNT hybrid nanostructure. The high performances of the developed sensors make them suitable for monitoring unhealthy actions (e. g. smoking, drinking coffee) in breastfeeding women and environmental factors (bad air quality), which are associated with an enhanced risk for SIDS.

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Lecoq, I., E. Mallet, JB Bonte, and G. Travert. "The A985 to G mutation of the medium-chain acyl-CoA dehydrogenase gene and sudden infant death syndrome in Normandy." Acta Paediatrica 85, no. 2 (February 1996): 145–47. http://dx.doi.org/10.1111/j.1651-2227.1996.tb13980.x.

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38

Park, M. R., S. K. Cho, J. Y. Park, K. M. Kim, Y. J. Choi, D. N. Kwon, K. C. Hwang, U. H. Tae, W. J. Son, and S. S. Paik. "65RARE AND OFTEN UNRECOGNIZED CEREBROMENINGITIS AND HEPATOPNEUMONIC CONGESTION ARE MAJOR CAUSES OF SUDDEN DEATH IN CLONED MALE PIGLETS." Reproduction, Fertility and Development 16, no. 2 (2004): 154. http://dx.doi.org/10.1071/rdv16n1ab65.

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In this study, we investigated the relationship between the sex of cloned pigs and sudden infant death syndrome (SIDS). Three cell lines (2 male and 1 female) were obtained from F1 fetuses derived from 3 different dams (Yorkshire) inseminated by the same sire (Landrace); one female fibroblast cell line was obtained from a Duroc-strain fetus acquired from a slaughterhouse, the age of the fetus unknown. The fetal fibroblast cells were cultured in DMEM supplemented with 10% fetal bovine serum under 5% CO2 in air at 37°C. For NT, we used the 4 cell lines described above. All 37 cloned piglets derived from 10 pregnant recipients were alive at term and began breathing readily. Of those piglets born, 18/22 males and 5/15 females died within 2 months of age. A total of 350 paraffin blocks from 18 deceased cloned male piglets and 90 paraffin blocks from six age-matched normal control piglets were prepared from the midbrain, medulla oblongata, liver, lung, kidney, spleen, small and large intestine, thymus, uterus, placenta, ovary, testis, skin, and skeletal muscle. We found that the birth weights of male clones were 57% lower than those of control age- and sex-matched piglets. Piglets with low birth weight (<900g) had more than twice the risk of SIDS relative to those piglets weighing more than 1000g. The low birth weights of the cloned male piglets (0.84±0.05kg) were not merely an artifact, as the average birth weights of cloned female piglets (1.47±0.09kg) were not lower than weights of piglets produced by AI-derived control female piglets (1.36±0.12kg). An initial examination of brain samples from 18 cloned male piglets that died soon after birth identified seven piglets with meningitis characterized by severe neutrophilic inflammation in the temporal brain lobes (38.8%, 7/18). We verified meningitis when more than 1000 neutrophils were counted per cubic millimeter of tissue. Next, we found hepatopneumonic congestion (16.6%, 3/18). The deceased male clones with meningitis showed extensive neuronal cell death and blood-brain barrier damage, whereas cloned piglets with congestion had fewer and larger alveolar air sacs. Extensive alveolar cell death, especially of pneumocytes and the bronchial epithelium, was confirmed by TUNEL assay. Lung and liver congestion may be caused by a slowly flowing blood stream from heart, resulting in CO2 and O2 exchange problems. Although the gross anatomy of the cloned male piglets was normal, they were associated with other severe handicaps, the commonest being leg abnormality which occurred in 33% (6/18) of dead male cloned piglets followed by Leydig cell hypoplasia and short face. Even though 4 of 41 AI-derived control piglets died within 1 week after birth, we could not find any anomalies in them. Thus, the present study suggests that our data might reflect sex difference but not cell type difference, and that death of the cloned male piglets might be caused by risk factors of sudden infant death syndrome such as low birth weight and multiple organ failure in conjunction with hepatopneumonic congestion and cerebromeningitis.

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39

Wang, S. S., P. M. Fernhoff, and M. J. Khoury. "Is the G985A Allelic Variant of Medium-Chain Acyl-CoA Dehydrogenase a Risk Factor for Sudden Infant Death Syndrome? A Pooled Analysis." PEDIATRICS 105, no. 5 (May 1, 2000): 1175–76. http://dx.doi.org/10.1542/peds.105.5.1175.

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40

Duran, M., L. Bruinvis, D. Ketting, J. B. de Klerk, and S. K. Wadman. "Cis-4-decenoic acid in plasma: a characteristic metabolite in medium-chain acyl-CoA dehydrogenase deficiency." Clinical Chemistry 34, no. 3 (March 1, 1988): 548–51. http://dx.doi.org/10.1093/clinchem/34.3.548.

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Abstract The profile of organic acids in plasma of patients with a deficiency of medium-chain acyl-CoA dehydrogenase (EC 1.3.99.3) was determined by gas-liquid chromatography of trimethylsilylated derivatives of the acids isolated by ethyl acetate extraction. All 13 patients had increased concentrations of free octanoate, cis-4-decenoate, and decanoate in their plasma. Cis-4-decenoate, an intermediary metabolite of linoleic acid, is pathognomonic of medium-chain acyl-CoA dehydrogenase deficiency. This metabolite does not accumulate in plasma after oral loading with medium-chain triglycerides, in contrast to octanoate and decanoate. Two postmortem plasma samples from victims of infant sudden-death syndrome had detectable octanoate and decanoate, but cis-4-decenoate could not be detected. The identification of cis-4-decenoate in plasma may be an aid in the diagnosis of an inherited defect in oxidation of medium-chain fatty acids.

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41

Buchanan, Gordon F., Haleigh R. Smith, Amanda MacAskill, and George B. Richerson. "5-HT2A receptor activation is necessary for CO2-induced arousal." Journal of Neurophysiology 114, no. 1 (July 2015): 233–43. http://dx.doi.org/10.1152/jn.00213.2015.

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Hypercapnia-induced arousal from sleep is an important protective mechanism pertinent to a number of diseases. Most notably among these are the sudden infant death syndrome, obstructive sleep apnea and sudden unexpected death in epilepsy. Serotonin (5-HT) plays a significant role in hypercapnia-induced arousal. The mechanism of 5-HT's role in this protective response is unknown. Here we sought to identify the specific 5-HT receptor subtype(s) involved in this response. Wild-type mice were pretreated with antagonists against 5-HT receptor subtypes, as well as antagonists against adrenergic, cholinergic, histaminergic, dopaminergic, and orexinergic receptors before challenge with inspired CO2 or hypoxia. Antagonists of 5-HT2A receptors dose-dependently blocked CO2-induced arousal. The 5-HT2C receptor antagonist, RS-102221, and the 5-HT1A receptor agonist, 8-OH-DPAT, attenuated but did not completely block CO2-induced arousal. Blockade of non-5-HT receptors did not affect CO2-induced arousal. None of these drugs had any effect on hypoxia-induced arousal. 5-HT2 receptor agonists were given to mice in which 5-HT neurons had been genetically eliminated during embryonic life ( Lmx1b f/f/p) and which are known to lack CO2-induced arousal. Application of agonists to 5-HT2A, but not 5-HT2C, receptors, dose-dependently restored CO2-induced arousal in these mice. These data identify the 5-HT2A receptor as an important mediator of CO2-induced arousal and suggest that, while 5-HT neurons can be independently activated to drive CO2-induced arousal, in the absence of 5-HT neurons and endogenous 5-HT, 5-HT receptor activation can act in a permissive fashion to facilitate CO2-induced arousal via another as yet unidentified chemosensor system.

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42

Lundemose, Jytte B., Niels Gregersen, Steen Karlvraa, Bent Nerrgaard Pedersen, Markil Gregersen, Karin Helweg-Larsen, and Jarrn Simonsen. "The frequency of a disease-causing point mutation in the gene coding for medium-chain acyl-CoA dehydrogenase in sudden infant death syndrome." Acta Paediatrica 82, no. 6-7 (June 1993): 544–46. http://dx.doi.org/10.1111/j.1651-2227.1993.tb12749.x.

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43

Wang, S. S., and M. J. Khoury. "An epidemiologic assessment of the relationship between the G985A medium chain acyl-coA dehydrogenase deficiency (MCADD) allelic variant and sudden infant death syndrome (SIDS)." Genetics in Medicine 1, no. 2 (February 1999): 43. http://dx.doi.org/10.1097/00125817-199901000-00017.

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44

Gozal, David, Evelyne Gozal, Stephen R. Reeves, and Andrew J. Lipton. "Gasping and autoresuscitation in the developing rat: effect of antecedent intermittent hypoxia." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1141–44. http://dx.doi.org/10.1152/japplphysiol.00972.2001.

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Gasping is a critically important mechanism for autoresuscitation and survival during extreme tissue hypoxia. Evidence of antecedent hypoxia in sudden infant death syndrome suggests that intermittently occurring hypoxic episodes may modify gasping and autoresuscitation. To examine this issue, an intermittent hypoxia (IH) profile consisting of alternating room air and 10% O2-balance N2 every 90 s was applied to pregnant Sprague-Dawley rats (IHRA; n = 50) and to pups after a normal pregnancy (RAIH; n = 50) as well as to control pups (RARA; n = 50). At postnatal day 5, pups were exposed to 95% N2-5% CO2, and gasping and the ability to autoresuscitate were assessed. Compared with RARA, IHRA- and RAIH-exposed pups had a reduced number of gasps, decreased overall gasp duration, and were less likely to autoresuscitate on introduction of room air to the breathing mixture during the last phase of gasping ( P < 0.001 vs. RARA). We conclude that both prenatal and early postnatal IH adversely affect gasping and related survival mechanisms.

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45

Cummings, Kevin J., Kathryn G. Commons, Julie C. Hewitt, John A. Daubenspeck, Aihua Li, Hannah C. Kinney, and Eugene E. Nattie. "Failed heart rate recovery at a critical age in 5-HT-deficient mice exposed to episodic anoxia: implications for SIDS." Journal of Applied Physiology 111, no. 3 (September 2011): 825–33. http://dx.doi.org/10.1152/japplphysiol.00336.2011.

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Mice deficient in the transcription factor Pet-1−/− have a ∼70% deficiency of brainstem serotonin [5-hydroxytryptamine (5-HT)] neurons and exhibit spontaneous bradycardias in room air at postnatal day (P)5 and P12 and delayed gasping in response to a single episode of anoxia at P4.5 and P9.5 (Cummings KJ, Li A, Deneris ES, Nattie EE. Am J Physiol Regul Integr Comp Physiol 298: R1333–R1342, 2010; and Erickson JT, Sposato BC. J Appl Physiol 106: 1785–1792, 2009). We hypothesized that at a critical age Pet-1−/− mice will fail to autoresuscitate during episodic anoxia, ultimately dying from a failure of gasping to restore heart rate (HR). We exposed P5, P8, and P12 Pet-1−/− mice and wild-type littermates (WT) to four 30-s episodes of anoxia (97% N2-3% CO2), separated by 5 min of room air. We observed excess mortality in Pet-1−/− only at P8: 43% of Pet-1−/− animals survived past the third episode of anoxia while ∼95% of WT survived all four episodes ( P = 0.004). No deaths occurred at P5 and at P12, and one of six Pet-1−/− mice died after the fourth episode, while all WT animals survived. At P8, dying Pet-1−/− animals had delayed gasping, recovery of HR, and eupnea after the first two episodes of anoxia ( P < 0.001 for each); death ultimately occurred when gasping failed to restore HR. Both high- and low-frequency components of HR variability were abnormally elevated in dying Pet-1−/− animals following the first episode of anoxia. Dying P8 Pet-1−/− animals had significantly fewer 5-HT neurons in the raphe magnus than surviving animals ( P < 0.001). Our data indicate a critical developmental window at which a brainstem 5-HT deficiency increases the risk of death during episodes of anoxia. They may apply to the sudden infant death syndrome, which occurs at a critical age and is associated with 5-HT deficiency.

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46

Curran, A. K., L. Xia, J. C. Leiter, and D. Bartlett. "Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 98, no. 3 (March 2005): 780–86. http://dx.doi.org/10.1152/japplphysiol.00906.2004.

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Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3–15 days. Blood pressure, end-tidal CO2, body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by ∼2.5°C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR.

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47

Davis, Joseph H. "Sudden Infant Death Syndrome." Pediatric Pathology & Laboratory Medicine 15, no. 2 (January 1995): 359–61. http://dx.doi.org/10.3109/15513819509026971.

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48

Carroll, J. L., and G. M. Loughlin. "Sudden Infant Death Syndrome." Pediatrics in Review 14, no. 3 (March 1, 1993): 83–93. http://dx.doi.org/10.1542/pir.14-3-83.

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49

Kim, Chang-Hwi. "Sudden Infant Death Syndrome." Journal of the Korean Medical Association 44, no. 9 (2001): 976. http://dx.doi.org/10.5124/jkma.2001.44.9.976.

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50

Fleming, Peter, and Peter S. Blair. "Sudden Infant Death Syndrome." Sleep Medicine Clinics 2, no. 3 (September 2007): 463–76. http://dx.doi.org/10.1016/j.jsmc.2007.05.003.

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