SUDDEN INFANT DEATH SYNDROME (SIDS)

Updated October 23, 1998

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What is Sudden Infant Death Syndrome (SIDS)?

SIDS is an unexpected sudden death of an infant in which a thourough postmortem investigation fails to demonstrate an adequate cause for death.

In sleep medicine, SIDS is classified as a parasomnia that cannot be classified in other sections. Infant breathing disorders are also included in the parasomnia section because newborns and young infants sleep a great portion of the day, and the majority of infant apnea and related respiratory disorders are observed while asleep. Apnea, congenital central hypoventilation syndrome, and periodic breathing are inborn features of infancy that reflect immaturity of the respiratory system rather than caused by a disease.

While there is general agreement that apnea associated with prematurity requires diagnosis, surveillence, and treatment, there is far less agreement about the boundaries between abnormal and normal display of sleep-related respiratory instabilities in term infants or premature infants who have reached 37 weeks' post-conceptional age.

The clinical significance of congential central hypoventilation and obstructive apnea due to a narrow airway is beyond doubt; however, controversy about the significance of other sleep apnea and breathing patterns is of such a magnitude that some doctors will be concerned, while others will view the same infant as healthy and the observed phenomena a variation of normal. The fear that respiratory instablility during sleep may predispose some infants to sudden infant death syndrome confers urgency to clinical management.

The majority of sudden infant death syndrome cases happen during a time the infant is presumed to be asleep. However, even though infant sleep apnea has been implicated as aprecursor to SIDS, there is no definite proof of a direct link.

Are there any symptoms?

Unfortunately, there are no outward symptoms. A seemingly healthy infant is put to bed and dies in his or her sleep. SIDS usally occurs in infants under 12 months of age. Rare cases occur between 12 and 24 months.

What we know:

Sleep-induced arrhythmias (loss of rhythm in the heart) may be a factor in SIDS. It has been hypothesized that changes in autonomic nervous system activity (The autonomic nervous system controls smooth muscle of the viscera (internal organs) and glands.) during sleep could precipitate an arrhythmia resulting in sudden death. Some potential abnormalities of autonomic function that might initiate a cardiac arrhythmia and SIDS have been reviewed by Verrier and Kirby. Although increased vagal tone (refers to the vagus nerve) is thought to have antiarrhythmic properties, it is possible that excess vagal tone that might occur during episodes of apnea could lead to profound bradycardia (slowness of the heartbeat) and asytole (cardiac standstill).

Guilleminault has observed significant bradycardia or sinus arrest in 38 of 594 infants studied following an episode of near-miss SIDS. In the vast majority of these subjects the arrhythmias observed during sleep were secondary to apnea and hypoventilation. Another possible mechanism of sudden cardiac death in SIDS victims is ventricular tachycardia (VF) (rapid heartbeat) secondary to increased sympathetic nervous system activity during REM sleep. Against this hypothesis is the absence of any documented abnormalities of the myocardium (the middle layer of the heart, consisting of heart muscle) or conduction system in victims of SIDS. In addition, ventricular arrhythmias have been infrequently observed in infants following an episode of near-miss SIDS.

A third possible mechanism of SIDS is a developmental imbalance of the autonomic nervous system, which could lead to inhomogeneity of depolarization (the destruction, neutralization, or change in polarity) and repolarization (the process in which the membrane, after depolarization, is polarized again, with positive charges on the outer and negative charges on the inner surface) within the myocardium.

Kralios and Millar have studied the functional development of cardiac sympathetic nerves in puppies between 1 and 6 weeks of age. These investigators observed a regression of functional maturation of all nerves except for the ventrolateral branch of the left stellate (star shaped) ganglion (nerve) in the third week of life. If regional sympathetic imbalance with left sympathetic predominance does develop at some point during maturation, this might provide the basis for the development of VF. Such a change might explain the prolongation of the QT interval (a measure of ventricular repolarization) that occurs in normal infants between 2 and 4 months of age. Although ventricular tachy-arrhythmia associated with prolongation of the QT interval has been proposed as a potential mechanism of SIDS, significant prolongation of the QT interval has not been documented in 100 infants studied following near-miss SIDS. Howeverm in support of the developmental imbalance hypothesis are the observations by several investigators of decreased heart rate variability during NREM sleep in near-miss SIDS victims and in the siblings of SIDS victims. Asimilar decrease in heart rate variability has been observed in patients who are at high risk of sudden cardiac death following myocardial infarction (an area of the heart muscle, usually due to the blocking of a coronary artery).

Thus, changes in the autonomic tone that occur during sleep could precipitate life-threatening cardiac arrhythmias in infants through several mechanisms. However, their role in SIDS is unknown.


Diagnostic Classification Steering Committee, Thorpy MJ, Chairman. International Classification of Sleep Disorders: Diagnostic and Coding Manual. Rochester, Minnesota: American Sleep Disorders Association, 1990.

Kryger, Meir H., Roth, Thomas, Dement, William C. Principles and Practice of Sleep Medicine, 2nd Edition. Philadelphia, Pennsylvania: W.B. Saunders Company, 1994.

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