eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
Current issue Archive Manuscripts accepted About the journal Special issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
2/2005
vol. 1
 
Share:
Share:
more
 
 

Review paper
Sudden infant death syndrome, prematurity and sleeping position

Harish Rao
,
Anne Greenough

Arch Med Sci 2005; 1, 2: 75-79
Online publish date: 2005/09/21
Article file
- Sudden infant.pdf  [0.06 MB]
Get citation
ENW
EndNote
BIB
JabRef, Mendeley
RIS
Papers, Reference Manager, RefWorks, Zotero
AMA
APA
Chicago
Harvard
MLA
Vancouver
 
 
Submitted: 12 June 2005
Accepted: 22 July 2005



Corresponding author:
Prof. Anne Greenough
Departmentt of Child Health
Guy’s, King’s and St Thomas’ School of Medicine
King’s Denmark Hill Campus
Bessemer Road
London, SE5 9PJ
Phone: 020 7346 30 37
Fax: 020 7346 82 84
E-mail: anne.greenough@kcl.ac.uk





Introduction
Sudden Infant Death Syndrome (SIDS) is the unexpected death of an infant occurring during the first months after birth, which remains unexplained after thorough investigation, including review of the clinical history, examination of death scene and a postmortem [1]. SIDS is the most common cause of post neonatal mortality and, in industrialized countries, accounts for 40% of all deaths from one month to one year of age [2]. The incidence of SIDS peaks between the second and fifth months after birth; ninety percent of the deaths from SIDS occur by six months of age. Certain infants are at an increased risk of SIDS (Table I) and include those slept prone. As a consequence, there have been national campaigns, such as “Back to Sleep”, aimed at reducing prone sleeping. These have resulted in a dramatic reduction in the incidence of SIDS. In the United Kingdom, the SIDS incidence decreased from 1.5-2.0/1000 live births in the mid 1980s to 0.5/1000 live births in 2000 and in the United States from 1.2 per 1000 live births in 1992 to 0.67 deaths per 1000 live births in 1999 [3]. Yet despite all the publicity, some infants, particularly those born prematurely, are still slept prone. In one series, only 35% of the prematurely born infants were slept non-prone at a corrected age of two months [4]. It is, therefore, important to understand why infants die of SIDS and prematurely born infants are at an increased risk, particularly if they are slept prone. Such information may help to convince parents and care givers that infants, particularly those born prematurely, should not be slept prone at the high-risk age for SIDS. The aims, then, of this review are to discuss possible causes of SIDS, describe the relationship of SIDS to premature birth and highlight the effects of prone sleeping position on prematurely born infants.

Possible causes of SIDS
Failure of arousal

Polygraphic studies have demonstrated that arousals were less common in infants who later died of SIDS than matched control infants [5]. Any impairment in respiratory control and/or arousability could then contribute to processes leading to SIDS [6]. Impaired arousal has been described during sleeping in the prone position and in infants who have been exposed to maternal smoking. Studies have consistently shown that sleeping prone increases the total amount of time spent asleep and, in particular, the amount of quiet sleep and is associated with a decreased number and duration of spontaneous arousals [6]. Healthy term born infants, regardless of their usual sleeping position, were demonstrated to sleep longer with a greater duration of non-rapid eye movement sleep and less arousals in the prone compared to the supine position when studied at three months of age [6]. In addition, arousal thresholds were significantly higher in both active and quiet sleep when term born infants were studied sleeping prone at two to three months of age [6].

Many studies have demonstrated a strong association between prenatal maternal smoking and SIDS [7]; the effect of smoking is dose dependent. The increase in risk of SIDS in infants whose mothers smoked during pregnancy is between two to four fold, but as high as six fold if there are other risk factors [8-10]. A possible mechanism for this increased risk is poorer arousal, exposure to cigarette smoke has been demonstrated to decrease both spontaneous and evoked arousals from sleep [11]. Premature babies born to mothers who smoked during pregnancy have been shown to have markedly decreased arousals and more apneas during active sleep [12]. Infants whose mothers smoked during pregnancy may have reduced chemoreceptor function; we have demonstrated that such infants have a dampened ventilatory response to added dead space [13]. This may be a manifestation of neurodevelopmental abnormalities in the control of ventilation resulting from prenatal nicotine exposure [14]. Prenatal nicotine exposure results in cell death in the brainstem of animal models [15]. The abnormalities could result from fetal hypoxia, as nicotine is a powerful vasoconstrictor and reduces blood flow to the uterus, as well as having a direct vasoconstrictor effect on the fetus [16]. In addition, fetuses of smoking mothers have raised carboxyhaemoglobin levels, resulting in a decrease in fetal oxygen tension, a shift in the oxygen dissociation curve to the left and a decrease in oxygen delivery to the tissues [17-19]. Nicotine is also a specific neuroteratogen; exposure to nicotine during critical phases of central nervous development resulted in abnormalities of cell replication, cell differentiation and receptor function in rats [20-22].

Infection
The likelihood that infection plays a part in SIDS is suggested by a number of observations, these include the increased (two to three times) incidence of SIDS in the winter months [23] and the high rate of concurrent upper respiratory infections in infants dying of SIDS. Infection changes both the amount and nature of sleep, with increases in both the duration and depth of quiet sleep; in addition, arousability from quiet sleep was found to be depressed after recent illness [24]. Infection may also be a stress factor that contributes to the death of an already vulnerable infant [23].
Genetic predisposition
Infants may be at increased risk of SIDS because they have mutations leading to genetic disorders capable of causing death [25]. For example, a testis-specific Y-like gene (TSPYL) localized to chromosome 6q22 has been found in nine families of the Belleville Amish community, the affected infants, who seemed normal at birth, developed signs of viscero-autonomic dysfunction early in life and died suddenly before 12 months of age [26].

Infants may also be at increased risk of SIDS as they have polymorphisms that might predispose to death in critical situations, that is gene environment interactions [25, 27]. The A985G mutation in medium chain acyl-coA dehydrogenase deficiency, the sodium channel gene (SCN5A) and the serotonin transporter gene mutations are a few examples of such polymorphisms. Genetic polymorphisms in fatty acid oxidation have also been estimated to be present in as many as five per cent of SIDS victims [28]. SCN5A polymorphisms in cardiac ion channels and the potential for lethal arrhythmia from long QT syndrome may result in SIDS. Indeed, it has been noted that certain infants who died of SIDS had a higher level of cardiac conduction abnormalities than infants who died of explained deaths [29] and a correlation has been found between long QT syndrome and SIDS in a subset of deaths [30, 31]. It has been estimated that between four and five percent of SIDS deaths may be associated with SCN5A polymorphisms. The serotonin transport gene was the first gene linked to SIDS vulnerability. Serotonin influences a broad range of physiologic systems, including the regulation of breathing, temperature and sleep-wake cycle and serotonergic receptor binding in the arcuate nucleus, nucleus raphe obscurus, and other medullary regions has been demonstrated to be decreased in SIDS cases [32].

Prematurity and SIDS
Prematurely born infants account for between 10 and 20% of SIDS cases. Infants born prior to 33 weeks of gestation are sixteen times more likely to die of SIDS than infants born at term. The incidence of SIDS is inversely related to gestational age at birth; the relative risk of SIDS in infants born at prior to 28 weeks of gestation being 3.6, but 1.7 in infants born between 34 and 36 weeks of gestational age [33, 34].

Prematurely born infants
and effect of sleeping position
Advantages of prone sleeping

Prematurely born infants with respiratory distress have better oxygenation, higher tidal volumes and lung compliance and lower respiratory rates and pulmonary resistance when nursed prone [35]. Immediately following extubation form mechanical ventilation, preterm infants nursed prone rather that supine have been demonstrated to have improved oxygenation, as they have less ventilation perfusion mismatch and asynchronous chest wall movement. The better thoraco-abdominal synchrony in the prone position is due to alterations in chest wall mechanics and respiratory muscle performance. The prone position also has advantages for preterm infants without respiratory distress [36], as they too have higher tidal volumes and more compliant lungs in the prone position. Such infants also have a reduced frequency of central and mixed apnoeas, bradycardias and desaturations when nursed prone. The higher rates of apnoea in the supine position may be due to neck flexion resulting in upper airway obstruction [37]. There is also less gastro-esophageal reflux in the prone position.

There have been few studies of the effect of sleeping position on convalescent prematurely born infants, those that have been undertaken still demonstrate benefits of prone positioning. These benefits include less apnoeas and periodic breathing [38] and superior oxygenation [39]. Amongst prematurely born infants being studied for discharge home, however, the benefit of prone positioning with regard to oxygenation was only seen in infants with chronic lung disease who were still oxygen dependent [40].

Disadvantages of prone sleeping
Healthy preterm infants born at a gestational age of 28 to 34 weeks studied at 12 to 57 days slept more in the prone position [41] and asymptomatic infants with a mean gestational age of 32 weeks studied at 36 weeks PMA had more quiet sleep and less awakenings in the prone position [42]. We have recently demonstrated that very prematurely born infants studied at 36 weeks PMA slept longer, spent more time in quiet sleep, had fewer arousals and had more central apnoeas in the prone position [43].

SIDS, prematurity and sleeping position
Prematurely born infants slept non-supine are at a much increased risk of SIDS. The odds ratio for SIDS in a prematurely born infant slept prone is 48.8 and side slept is 40.5 [44].

Advice to parents
As a consequence of the increased risk of SIDS if prematurely born infants are slept prone, it is clearly important that parents are advised against such a practice. Yet a survey of all neonatal units in the United Kingdom demonstrated that, although all recommended supine sleeping on discharge from the neonatal unit, approximately forty percent did not discourage prone sleeping [45]. In addition, some additionally recommended side sleeping, although this also has an increased risk of SIDS for prematurely born infants. This inappropriate advice may reflect that clinicians appreciate that prone sleeping has advantages for prematurely born infants in the first weeks after birth as documented above and, also, the then lack of data regarding the effect of sleeping position in prematurely born infants at discharge and at the high risk age for SIDS.

Conclusion
We have recently demonstrated that prone positioning of prematurely born infants at 36 weeks PMA is associated with greater sleep efficiency, more central apnoeas and less arousals [43]. As a consequence, we recommend that prematurely born infants are slept supine at least at that post menstrual age. Such a practice will mean that oxygen dependent infants will require more supplementary oxygen [40]. Parents need to be appropriately supported and counseled that such a disadvantage is far outweighed by the reduced risk for SIDS.
References
1. Guffanti S, Grancini F, Scalfaro C, Podesta AF. Sudden infant death syndrome (SIDS). Pediatr Med Chir 2004; 26 (2): 96-104.
2. Willinger M. SIDS prevention. Pediatr Ann 1995; 24 (7): 358-64.
3. Moon RY, Oden RP, Grady KC. Back to Sleep: an educational intervention with women, infants, and children program clients. Pediatrics 2004; 113: 542-7.
4. Adams MM, Kugenen B, Mirmiran M, Ariagno RL. Survey of sleeping position after hospital discharge in healthy preterm infants. J Perinatol 1988; 18: 168-72.
5. Kato I, Franco P, Groswasser J, Scallier S, Kelmanson I, Togari H, et al. Incomplete arousal processes in infants who were victims of sudden death. Am J Respir Crit Care Med 2003; 168: 1298-303.
6. Horne RS, Parslow PM, Harding R. Respiratory control and arousal in sleeping infants. Paediatr Respir Rev 2004; 5 (3): 190-8.
7. DiFranza JR, Aligne CA, Weitzman M. Prenatal and postnatal environmental tobacco smoke exposure and children’s health. Pediatrics 2004; 113 (4 suppl.): 1007-15.
8. Chong DS, Yip PS, Karlberg J. Maternal smoking: an increasing unique risk factor for sudden infant death syndrome. Acta Pediatr 2004; 93: 450-2.
9. Mitchell EA, Tuohy PG, Brunt JM, Thompson JM, Clements MS, Stewart AW, et al. Risk factors for sudden infant death syndrome following the prevention campaign in New Zealand. Pediatrics 1997; 100: 835-40.
10. Williams SM, Mitchell EA, Taylor BJ. Are risk factors for sudden infant death syndrome different at night? Arch Dis Child 2002; 87: 274-8.
11. Horne RS, Franco P, Adamson TM, Groswasser J, Kahn A. Influences of maternal cigarette smoking on infant arousability. Early Hum Dev 2004; 79 (1): 49-58.
12. Sawnani H, Jackson T, Murphy T, Beckerman R, Simakajornboon N. The effect of maternal smoking on respiratory and arousal patterns in preterm infants during sleep. Am J Respir Crit Care Med 2004; 169 (6): 733-8.
13. Bhat R, Broughton S, Khetriwal B, Rafferty GF, Hannam S, Milner AD, et al. Dampened ventilatory response to added deadspace in newborns of smoking mothers. Arch Dis Child 2005 (in press).
14. Lewis KW, Bosque EM. Deficient hypoxia awakening response in infants of smoking mothers: Possible relationship to sudden infant death syndrome. J Pediatr 1995; 127: 6919-33.
15. Krous HF, Campbell GA, Fowler MW, Catron AC, Farber JP. Maternal nicotine administration and fetal brainstem damage: a rat model with implication for sudden infant death syndrome. Am J Obstet Gynaecol 1981; 140: 743-6.
16. Suzuki K, Minei LJ, Johnson EE. Effect of nicotine upon uterine blood flow in the pregnant Rhesus monkey. Am J Obstet Gynecol 1980; 136: 1009-13.
17. Bureau MA, Shapcott D, Berthiaume Y, Monette J, Blouin D, Blanchard P, et al. Maternal cigarette smoking and fetal oxygen transport: a study of P50,2,3-diphosphoglycerate, total haemoglobin, hematocrit and type F in fetal blood. Pediatrics 1983; 72: 22-6.
18. Longo LD. The biological effects of carbon monoxide on the pregnant woman, fetus and newborn infant. Am J Obstet Gynecol 1977; 129: 69-103.
19. Longo LW. Carbon dioxide: effects on oxygenation of the fetus in utero. Science 1976; 194: 522-4.
20. McFarland BJ, Seidler FJ, Slotkin TA. Inhibition of DNA synthesis in neonatal rat brains regions caused by acute nicotine exposure. Dev Brain Res 1991; 58: 223-9.
21. Seidler FJ, Levin ED, Lappi SE, Slotkin TA. Fetal nicotine exposure ablates the ability of postnatal nicotine challenge to release norepinephrine from rat brain regions. Dev Brain Res 1992; 69: 288-91.
22. Zahalka EA, Seidler FJ, Lappi SE, McCook EC, Yanai J, Slotkin TA. Deficits in development of central cholinergic pathways caused by fetal nicotine exposure: differential effects on choline acetyltransferase activity and (3H) Hemicholinium-3 binding. Neurotoxicol Teratol 1992; 14: 375-82.
23. Byard RW, Krous HF. Sudden infant death syndrome: overview and update. Pediatr Dev Pathol 2003; 6 (2): 112-27.
24. Horne RS, Osborne A, Vitkovic J, Lacey B, Andrew S, Chau B, et al. Arousal from sleep in infants is impaired following an infection. Early Hum Dev 2002; 66 (2): 89-100.
25. Opdal SH, Rognum TO. The sudden infant death syndrome gene: does it exist? Pediatrics 2004; 114 (4): e506-e512.
26. Opdal SH, Rognum TO. New insight into sudden infant-death syndrome. Lancet 2004; 364: 825-6.
27. Hunt CE. Gene-environment interactions: implications for sudden unexpected deaths in infancy. Arch Dis Child 2005; 90 (1): 48-53.
28. Wood JC, Magera MJ, Rinaldo P, Seashore MR, Strauss AW, Friedman A. Diagnosis of very long chain acyl-dehydrogenase deficiency from an infant’s newborn screening card. Pediatrics 2001: 108 (1): E19.
29. Matturri L, Ottaviani G, Ramos SG, Rossi L. Sudden Infant Death Syndrome (SIDS): a study of cardiac conduction system. Cardiovasc Pathol 2000; 9 (3): 137-45.
30. Guntheroth WG, Spiers PS. Prolongation of the QT interval and the sudden infant death syndrome. Pediatrics 1999; 103: 813-14.
31. Schwartz PJ, Stramba-Badiale M, Segantini A, Austoni P, Bosi G, Giorgetti R, et al. Prolongation of the QT interval and the sudden infant death syndrome. N Engl J Med 1998; 338 (24): 1709-14.
32. Weese-Mayer DE, Berry-Kravis EM, Maher BS, Silvestri JM, Curran ME, Marazita ML. Sudden infant death syndrome: association with a promoter polymorphism of the serotonin transporter gene. Am J Med Genet A 2003; 117 (3): 268-74.
33. Kramer MS, Demissie K, Yang H, Platt RW, Sauve R, Liston R. The contribution of mild and moderate preterm birth to infant mortality. Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System. JAMA 2000; 284 (7): 843-9.
34. Spiers PS. The influence of race and gestational age on the age of maximum risk of SIDS in infancy. Med Hypotheses 2000; 55 (1): 51-5.
35. Mendoza JC, Roberts RL, Cook LN. Postural effects on pulmonary function and heart rate of preterm infants with lung disease. J Pediatr 1991; 118: 445-8.
36. Adams JA. Zabaleta I, Sackner MA. Comparison of supine and prone non-invasive measurements of breathing patterns in full term newborns. Pediatr Pulmonol 1994; 18 (1): 8-12.
37. Stark A, Thach B. Mechanisms of airway obstruction leading to apnoea in newborn infants. J Pediatr 1976; 89: 982-5.
38. Heimler R, Langlois J, Hodel D, Nelin LD, Sasidharan P. Effect of positioning on the breathing pattern of preterm infants. Arch Dis Child 1992; 67: 312-4.
39. Dimitriou G, Greenough A, Castling D, Kavvadia V. A comparison of supine and prone positioning in oxygen dependent and convalescent premature infants. Br J Intens Care 199; 6: 254-9.
40. Bhat RY, Leipala JA, Singh NR, Rafferty GF, Hannam S, Greenough A. Effect of posture on oxygenation, lung volume, and respiratory mechanics in premature infants studied before discharge. Pediatrics 2003; 112: 29-32.
41. Materson J, Zucker C, Schulze K. Prone and supine positioning effects on energy expenditure and behaviour of low birthweight neonates. Pediatrics 1987; 80: 689-902.
42. Goto K, Mirmiran M, Adams MM, Longford RV, Baldwin RB, Boeddiker MA, et al. More awakenings and heart rate variability during supine sleeping in preterm infants. Pediatrics 1999; 103: 603-9.
43. Bhat RY, Rafferty GF, Hannam S, Greenough A. Effect of posture on gastro-oesophageal reflux (GOR) and is association to apnoea in convalescent preterm infants. Eur Respir J 2004; 24 (48): 4237.
44. Oyen N, Markestad T, Skjaerven R, et al. Combined effects of sleeping position and prenatal risk factors in sudden infant death syndrome; the Nordic Epidemiological SIDS Study. Pediatrics 1997; 100: 613-21.
45. Bhat RY, Leipala JA, Rafferty GF, Hannam S, Greenough A. Survey of sleeping position recommendations for prematurely born infants on neonatal intensive care unit discharge. Eur J Pediatr 2003; 162 (6): 426-7.
Copyright: © 2005 Termedia & Banach. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2020 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe