A New Perspective on Sudden Infant Death Syndrome have long assumed that sudden infant death syndrome occurred in normal babies unexpectedly,1 that there was no means by which babies at risk for SIDS could be identified beforehand,2 and that the physician's role in management of SIDS commenced with the event of death and concerned itself only with supporting and counseling families of the victim.3 In this issue of the Journal (p 1207), Naeye and Drage (and Naeye elsewhere4) present evidence which indicates that babies who die of SIDS are not normal, that their deaths are not totally unexpected, and that physicians may indeed be able to predict those at risk and intervene to prevent such deaths. Their prospective, matched-control study strongly suggests that babies born in certain demographic circumstances, under certain antepartum influences, and with certain neonatal histories, physical findings, and behaviors are at higher risk for SIDS than babies who do not share these circumstances. As such, these variables may well be predictors of SIDS susceptibility. For instance, babies born to poor, young, unmarried moth¬ ers who have little education, live in crowded homes, smoke excessively, are anemic, and have a history of prior fetal losses and few prenatal visits are more likely to suffer SIDS. So too are babies who require resuscitation, posi¬ tive respiratory pressure, and open
We (SIDS)
oxygen, who develop respiratory dis¬ tress syndrome, and who receive anti¬
have initial difficulties with that feeding delay bottle feeding. Moreover, those born small for gesta¬ tional age who lose less weight than expected in the first 72 hours of life, who gain less rapidly than expected during their first few months of life, and who demonstrate diminished levels of behavioral response to a variety of environmental stimuli die more frequently from SIDS. There are other predictors including a variety of measurable neurological abnormali¬ ties. The authors postulate that a variety of antenatal factors produce neonatal central nervous system dysfunction, particularly in the brain stem, asso¬ ciated with dysregulation of the respi¬ ratory drive, apnea, and chronic hypoxia. This theory is consistent with the findings in histopathologic and cardiorespiratory studies per¬ formed in animals, on SIDS victims, and on infants with severe apneic biotics
spells.
or
Marx"' has reviewed the evidence at hand and, although careful not to draw hard and fast conclusions, she gives us the opportunity to see how the information we do have could, with further study, soon lead to reasonable conclusions regarding the long-sought pathophysiological mech¬ anisms in SIDS. It would seem that there are subtle physiological defects in the mechanisms that control
breathing the SIDS victims. These are
probably due to abnormal maturation of or injury to the respiratory centers in the brain stem caused by antepartum and postpartum noxious and
hypoxic influences. Immaturity dysregulation of the respiratory trol mechanisms
can
and con¬
then lead to
bradycardia, severe cardiac arrhythmias, and death under circum¬ stances in which a mature, normally functioning respiratory drive system apnea,
manages without untoward effects.
Hypoxia does produce histologie and chemical changes in the brain stem (proliferation of astroglial fi¬ bers, retarded formation of neurons, impaired synthesis of neurotransmitters), and a brain stem so affected responds sluggishly
to
respiratory
stimuli from mechanical and chemosensitive receptors in the upper larynx. These stimuli occur more frequently under circumstances that
produce momentary upper airway obstruction (respiratory infections, régurgitation, hypoglycemia, and ret-
romandibular movement). Infants who die of SIDS do demonstrate histo¬ logie changes consistent with chronic hypoxia (hypertrophy of the medial muscle mass in small pulmonary arteries, hepatic erythropoiesis, and prolonged retention of periadrenal brown fat). Frequent, prolonged ap¬ nea and anemia, or both, could explain these findings. The hypoxia producing these changes could also further adversely affect the brain stem respi-
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ratory control mechanisms—in essence a vicious cycle may be opérant.
Although these observations do not confirm the etiology of SIDS, they do provide substantial leads for further research to that end. Likewise, Naeye and Drage have suggested some mechanisms by which we may be able to predict susceptibility to SIDS. Their indicators are larger in number than those of Emery and Carpenter" (although there is some overlap), who were able to demonstrate a striking reduction in expected, unexpected deaths in infants so identified during their first 20 weeks of life. This was accomplished by following up at-risk infants closely through fortnightly visits to their homes by health visitors (public health nurses). Their results are impressive, but their method for
monitoring sive. Whether
predictors
is or
prohibitively
expen¬
Naeye and Drage's sufficiently reliable
not
are
remains to be seen. Their criteria must be applied to larger numbers of SIDS babies and shown to hold true before we can share our suspicions regarding increased risk for SIDS with the parents of these babies. To do so now on the basis of these indicators would create unwarranted anxiety. Moreover, until we find an effective and economical means by which to monitor those at risk in order to prevent SIDS, nothing would be gained by such action. We can and should, however, intervene in every way possible, through improved antepartum care, to reduce the risk for developing the physiologic defects
that
lead to SIDS. ROBERT A. HOEKELMAN, MD Department of Pediatrics University of Rochester School of Medicine and Dentistry 601 Elmwood Ave
can
Rochester,
NY 14642 References 1. Ray GC, Bergman AB, Beckwith JB: An analysis of the problem. Pediatr Ann 3:8-39,
1974. 2. Beckwith JB: The sudden infant death syndrome. Curr Probl Pediatr 3:31, 1973. 3. Hoekelman RA: The physician's responsibility in the management of sudden infant death syndrome. Am J Dis Child 128:16-17, 1974. 4. Naeye RL, Messmer J, Specht T, et al: Sudden infant death syndrome temperament before death. J Pediatr 88:511-515, 1976. 5. Marx JL: Crib death: Some promising leads but no solutions yet. Science 189:367-369, 1975. 6. Emery JL, Carpenter RG: Clinical aspects of the Sheffield prospective study of children at possibly increased risk, in SIDS 1974. Toronto, Canadian Foundation for the Study of Infant Death, 1974, pp 97-106.
Downloaded From: http://archpedi.jamanetwork.com/ by a DALHOUSIE UNIVERSITY-DAL-11762 User on 06/21/2015
We (SIDS)
oxygen, who develop respiratory dis¬ tress syndrome, and who receive anti¬
have initial difficulties with that feeding delay bottle feeding. Moreover, those born small for gesta¬ tional age who lose less weight than expected in the first 72 hours of life, who gain less rapidly than expected during their first few months of life, and who demonstrate diminished levels of behavioral response to a variety of environmental stimuli die more frequently from SIDS. There are other predictors including a variety of measurable neurological abnormali¬ ties. The authors postulate that a variety of antenatal factors produce neonatal central nervous system dysfunction, particularly in the brain stem, asso¬ ciated with dysregulation of the respi¬ ratory drive, apnea, and chronic hypoxia. This theory is consistent with the findings in histopathologic and cardiorespiratory studies per¬ formed in animals, on SIDS victims, and on infants with severe apneic biotics
spells.
or
Marx"' has reviewed the evidence at hand and, although careful not to draw hard and fast conclusions, she gives us the opportunity to see how the information we do have could, with further study, soon lead to reasonable conclusions regarding the long-sought pathophysiological mech¬ anisms in SIDS. It would seem that there are subtle physiological defects in the mechanisms that control
breathing the SIDS victims. These are
probably due to abnormal maturation of or injury to the respiratory centers in the brain stem caused by antepartum and postpartum noxious and
hypoxic influences. Immaturity dysregulation of the respiratory trol mechanisms
can
and con¬
then lead to
bradycardia, severe cardiac arrhythmias, and death under circum¬ stances in which a mature, normally functioning respiratory drive system apnea,
manages without untoward effects.
Hypoxia does produce histologie and chemical changes in the brain stem (proliferation of astroglial fi¬ bers, retarded formation of neurons, impaired synthesis of neurotransmitters), and a brain stem so affected responds sluggishly
to
respiratory
stimuli from mechanical and chemosensitive receptors in the upper larynx. These stimuli occur more frequently under circumstances that
produce momentary upper airway obstruction (respiratory infections, régurgitation, hypoglycemia, and ret-
romandibular movement). Infants who die of SIDS do demonstrate histo¬ logie changes consistent with chronic hypoxia (hypertrophy of the medial muscle mass in small pulmonary arteries, hepatic erythropoiesis, and prolonged retention of periadrenal brown fat). Frequent, prolonged ap¬ nea and anemia, or both, could explain these findings. The hypoxia producing these changes could also further adversely affect the brain stem respi-
Downloaded From: http://archpedi.jamanetwork.com/ by a DALHOUSIE UNIVERSITY-DAL-11762 User on 06/21/2015
ratory control mechanisms—in essence a vicious cycle may be opérant.
Although these observations do not confirm the etiology of SIDS, they do provide substantial leads for further research to that end. Likewise, Naeye and Drage have suggested some mechanisms by which we may be able to predict susceptibility to SIDS. Their indicators are larger in number than those of Emery and Carpenter" (although there is some overlap), who were able to demonstrate a striking reduction in expected, unexpected deaths in infants so identified during their first 20 weeks of life. This was accomplished by following up at-risk infants closely through fortnightly visits to their homes by health visitors (public health nurses). Their results are impressive, but their method for
monitoring sive. Whether
predictors
is or
prohibitively
expen¬
Naeye and Drage's sufficiently reliable
not
are
remains to be seen. Their criteria must be applied to larger numbers of SIDS babies and shown to hold true before we can share our suspicions regarding increased risk for SIDS with the parents of these babies. To do so now on the basis of these indicators would create unwarranted anxiety. Moreover, until we find an effective and economical means by which to monitor those at risk in order to prevent SIDS, nothing would be gained by such action. We can and should, however, intervene in every way possible, through improved antepartum care, to reduce the risk for developing the physiologic defects
that
lead to SIDS. ROBERT A. HOEKELMAN, MD Department of Pediatrics University of Rochester School of Medicine and Dentistry 601 Elmwood Ave
can
Rochester,
NY 14642 References 1. Ray GC, Bergman AB, Beckwith JB: An analysis of the problem. Pediatr Ann 3:8-39,
1974. 2. Beckwith JB: The sudden infant death syndrome. Curr Probl Pediatr 3:31, 1973. 3. Hoekelman RA: The physician's responsibility in the management of sudden infant death syndrome. Am J Dis Child 128:16-17, 1974. 4. Naeye RL, Messmer J, Specht T, et al: Sudden infant death syndrome temperament before death. J Pediatr 88:511-515, 1976. 5. Marx JL: Crib death: Some promising leads but no solutions yet. Science 189:367-369, 1975. 6. Emery JL, Carpenter RG: Clinical aspects of the Sheffield prospective study of children at possibly increased risk, in SIDS 1974. Toronto, Canadian Foundation for the Study of Infant Death, 1974, pp 97-106.
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