Effect on Sleep Position on Apnea and Bradycardia in High-Risk Infants

Here is a letter in the Medical Journal Nature in full. Interesting stuff about the origins of the SIDS and Sleep Apnea theory connection.


March 2002, Volume 22, Number 2, Pages 163-164
Commentary

Effect on Sleep Position on Apnea and Bradycardia in High-Risk Infants


Joan E Hodgman MD

Keck School of Medicine, USC Medical Center, University of Southern California, Los Angeles County, Los Angeles, CA, USA

Correspondence to: Joan E. Hodgman, MD, Women's and Children's Hospital, 1240 North Mission Road, Los Angeles, CA 90033, USA


Abstract


Journal of Perinatology (2002) 22, 163-164 DOI: 10.1038/sj/jp/7210658



Hershberger and associates1 recently published a careful study in the Journal of Perinatology of apnea and bradycardia during monitoring of infants considered at risk for SIDS in the prone and side-lying positions during sleep. They hypothesized that there would be increased cardiorespiratory events in the infants when prone. Their results did not bear this out as they found no differences. The expectation of differences was apparently based on the belief that apnea and SIDS are related. There have never been any convincing data linking apnea to SIDS.

The sleep apnea theory was proposed by Steinschneider2 in 1972 based on studies of five infants, two of whom died, with no controls. The cause of the deaths was later proven to be infanticide.3 This theory was rapidly embraced by both the medical and the lay public presumably because it offered the possibility of intervention by monitoring. In spite of widespread monitoring of infants in the United States during almost 30 years, monitoring has not decreased the rate of SIDS.4 Cardiorespiratory abnormalities in the pneumogram were reported to identify infants at risk for SIDS and consequently recommended for infants who should benefit from monitoring. These recommendations were never published in a peer-reviewed journal but rather by the SIDS Foundation, a predominantly lay organization of parents of SIDS infants. The abnormalities described are common in normal infants and the use of pneumograms for this purpose is no longer recommended.5

No studies have related the presence of apnea or bradycardia on monitoring with SIDS. Our own studies of infants following an apparent life-threatening event (ALTE) showed no such differences from controls.6 The extensive report by Southall et al.7 of recordings of infants discharged from a neonatal intensive care unit showed no relation between findings on the recordings and subsequent death. The recent publication of results from the Collaborative Home Infant Monitoring Evaluation (CHIME) study by Ramanathan and colleagues8 reported no differences between term infants at risk and controls. Premature infants had increased apnea and bradycardia only until 43 weeks, well before the peak incidence of SIDS.

There are few epidemiologic data to support the sleep apnea theory. Histories of infants dying of SIDS rarely contain reference to apnea.9 Premature infants are at greater risk for both early apnea and SIDS, but these appear related to maturity rather than directly to each other. In our large premature center, the risk of SIDS in infants of birth weigh <1500 g after discharge has been close to 1 per 100, but those who died were almost entirely asymptomatic in the nursery. Infants who suffered an ALTE due to apnea of prematurity have been reported to be at increased risk for SIDS.10,11 However, a number of the reported infants had two or more preceding familial deaths, which is considered to rule out SIDS in favor of infanticide. In fact, the use of previous terms for an ALTE such as near-miss for SIDS and aborted crib death have been abandoned as misleading. The etiology of apnea of infancy is as mysterious as that of SIDS itself. No studies have demonstrated a reduction in SIDS deaths following an ALTE attributable to monitoring.

The authors of the article under discussion did not elaborate on why they did not complete their study by including infants in the supine position. My hypothesis would be that no differences would be found in apnea and bradycardia between prone and supine positions. It is past time to put the sleep apnea theory to rest.


References


1 Hershberger ML, Peeke KL, Levett J, Spear ML. Effect of sleep position on apnea and bradycardia in high-risk infants. J Perinatol 2000; 21: 85-9.

2 Steinschneider A. Prolonged apnea and the sudden infant death syndrome: clinical and laboratory observations. Pediatrics 197; 50: 646-54.

3 Firstman R, Talan J. The Death of Innocents: A True Story of Murder, Medicine, and High Stakes Science New York: NY Bantam, 1997.

4 Davidson Ward SL, Keens TG, Chan LS et al. Sudden infant death syndrome in infants evaluated by apnea programs in California. Pediatrics 1986; 77: 451-5. MEDLINE

5 Consensus statement: National Institutes of Health Consensus Development Conference on Infantile Apnea and Home Monitoring, Sept 29 to Oct 1, 1986. Pediatr 1987; 79: 292-9.

6 Hodgman JE, Hoppenbrouwers T, Geidel S et al. Respiratory behavior in near-miss sudden infant death syndrome. Pediatrics 1982; 69: 785-92. MEDLINE

7 Southall DP, Richards JM, Rhoden KJ et al. Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: failure to predict an increased risk for sudden infant death syndrome. Pediatrics 1982; 70: 844-51. MEDLINE

8 Ramanathan R, Corwin MJ, Hunt CE et al. Cardiorespiratory events recorded on home monitors. Comparison of healthy infants with those at increased risk for SIDS. JAMA 2001; 285: 2199-2207. MEDLINE

9 Hoffman HJ, Damus K, Hillman L, Drongrad E. Risk factors for SIDS: results of the National Institute of Child Health and Human Development SIDS Cooperative Epidemiological Study. Ann NY Acad Sci 1988; 533: 112-30.

10 Oren J, Kelly D, Shannon DC. Identification of a high-risk group for sudden infant death syndrome among infants who were resuscitated for sleep apnea. Pediatrics 1986; 77: 495-9. MEDLINE

11 Schwartz PJ, Southall DP, Valdez-Idapena M. The Sudden death syndrome: cardiac and respiratory mechanisms and interventions. Ann NY Acad Sci 1988; 533: 1-474.