Infant Sleep Disorders
There are more than 80 ICD-9 classified sleep disorders, and scores of causes for both sleepiness and insomnia. Figure 1 illustrates the enormous variety of intrinsic and extrinsic factors that influence sleep disorder presentations on the developing child. Infant sleep is influenced by gestational age, environment, and parenting skills. Add to that the unique anatomy of an infant[1,2] combined with an immature nervous system, and infant sleep develops into a separate science in sleep medicine. Unlike apnea at other stages of development, sleep-disordered breathing in the infant presents a unique threat to life. Apnea of prematurity, infant apnea, and sudden infant death syndrome (SIDS) are all examples of disordered breathing or possibly disordered arousal during sleep. Extensive diagnostic evaluations of infant apnea and 30 years of apnea monitor use did not change the incidence of SIDS. New guidelines on infant apnea management and monitor use are but partially based on evidence underscoring the lack of mechanistic knowledge regarding vulnerability in these infants.
Long-term consequences of untreated childhood sleep problems. There are an enormous variety of intrinsic and extrinsic factors that influence sleep disorder presentations on the developing child. These factors can influence the subsequent stages of development.
In the past decade, attention to epidemiological evidence caused the first worldwide decline in the incidence of SIDS.[5,6] Efforts aimed at reducing modifiable risk factors related to SIDS, notably the prone sleeping position, over-bundling, and smoke exposure reduced the SIDS incidence by more than 60% in most parts of the world. Attention to the new epidemiology of SIDS cases has now demonstrated a similar risk profile for infants dying unexpectedly but of known causes such as medical disorders, with chaotic home environments and parental unemployment increasing the risk.
Sudden infant death syndrome is not a disease, but a symptom or outcome of an underlying problem. As SIDS victims decline, there is renewed focus on what is still killing the vulnerable infant, with both environmental and intrinsic mechanisms suggested. An apparent increase in the incidence of infanticide merely reflects its growing percentage in contrast to the declining postneonatal deaths. While the possibility of child abuse should no longer be ignored in infant death, investigation of the death scene, or more importantly, the sleep environment, is key to understanding what makes a child vulnerable and perhaps more importantly, what keeps a child alive. Mechanistic studies focusing on the known risk factors have shown that infants sleeping in the prone position re-breathe exhaled gas or have oxygenation problems and decreased arousal,[11,12,13] or a more collapsible pharynx, risking obstruction. Genetic alterations in the brainstem, cell function, or cytokine profile may cause vulnerability in some infants. Cigarette smoke and its apparent causal relation to SIDS has been an area of intense study with evidence for decreased arousal in smoke-exposed infants.[19,20]
There is a recent proposal for a new pathologic definition of SIDS. The term sudden infant death syndrome is an exclusionary term when a cause for death cannot be found. According to Dr. Beckwith, this term has been used too liberally, allowing deaths to be labeled SIDS when in fact no autopsy or death scene investigation was performed. Other pediatric pathologists agree that it is time for a new definition,[22,23] using lessons learned from epidemiological evidence, and also allowing for advances in cell and molecular biology to aid in research.
One cannot ignore the racial disparity in incidence of postneonatal deaths. Infant mortality statistics from 2000 yield a death rate for low birthweight African American infants four times that of white infants. The SIDS rate for black and Native American infants is more than twice that of white infants. Recent case control or questionnaire studies[25,26] have blamed an increase in prone positioning for the racial disparity in SIDS; however, other studies have demonstrated more of an impact from infant sleep on nonstandard sleep surfaces[27*,28] including bedsharing, which varies by culture. Bedsharing was very risky in a study of Native American infant deaths, which included a history of parental alcohol use, a risk factor noted in the CESDI/SUDI study referenced previously. The recently considered mechanism causing death in nonstandard bedding is deficient arousal to hypoxia or hypercapnia associated with a covered head, as can happen with soft bedding or thick blankets on adult beds. In a prospective study of 27,000 infants in Japan, an association between obstructive sleep apnea and gliosis in the raphe nuclei of the midbrain was found in SIDS cases, but its relation to arousal deficiency remains to be seen.
Although not life threatening, infant sleep rhythms affect infant and maternal well being. In a well-designed randomized controlled trial (RCT), infant sleep was reported as abnormal in 46% of visits to the pediatric clinic during the second 6 months of life. Early behavioral intervention decreased both sleep problems and maternal depression.[32*] In a separate RCT, sleep problems in infants were predicted in those infants who had a high number (>11) of feeds per day. A simple preventative behavioral program increased the number who slept through the night.
Curr Opin Pulm Med. 2003;9(6) © 2003 Lippincott Williams & Wilkins
Cite this: Sleep Disorders in Children - Medscape - Nov 01, 2003.