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Sudden infant death syndrome (SIDS) is the unexpected death of infants <1 year old for which no pathologic cause can be determined by a thorough history, physical examination, postmortem examination, and environmental investigation. SIDS is a diagnosis of exclusion. The syndrome has been a leading cause of death of infants between 1 month and 1 year of age. In the past, between 5000 and 10,000 infants (1 to 2 per 1000 live births) succumbed yearly to SIDS. With recent changes in infant sleep position, the number of deaths has decreased to about 3000, or 0.8 deaths per 1000 infants. In addition, the recognition of other risk factors, such as bed-sharing and parental smoking, have altered the way sudden unexpected deaths during infancy are categorized, and the number of SIDS cases may be, in part, related to this change in diagnostic criteria.1 Another term that is applicable to these infants is sudden unexplained infant death, which includes cases of SIDS.

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Pathophysiology

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The etiology and pathophysiology of SIDS remain unclear in spite of continued investigation. Over the years, >70 different theories have been proposed to explain SIDS, including suffocation from sleeping with a parent (overlaying), milk allergy, and thymic enlargement. Because most SIDS victims are found dead in their cribs, early theories emphasized the role of apnea and ventilatory control, as well as possible cardiac etiologies. Although cardiac dysfunction related to prolonged QT interval or Wolff-Parkinson-White syndrome have been reported,2prospective studies monitoring infants failed to show antecedent dysrhythmia in infants who subsequently succumbed to SIDS. More recent studies on the brains of infants who have died from SIDS demonstrate the presence of medullary serotonergic (5-hydroxytryptamine) pathology, including abnormal firing, synthesis, release, and clearance.3,4 Currently, emphasis is placed on the interplay between developmental factors related to autoregulation, arousal, and environmental stressors. The triple-risk model for SIDS3 hypothesizes a “perfect storm” of underlying vulnerability, a critical period of development, and exogenous stressors. The underlying vulnerability can include genetic factors, male gender, race, poverty, or prenatal exposure to cigarettes, alcohol, and illicit drugs. Although no single genetic locus for SIDS has been identified, the 10-fold increased risk among the siblings of SIDS victims suggests a genetic component. Recently, polymorphism in the interleukin-10 gene promoter has been associated with SIDS and sudden unexpected death associated with infection. The first 6 months of life represents a unique critical period of vulnerability. Potential external stressors include prone sleeping, soft or adult bedding, bed sharing, and minor infection, often with respiratory syncytial virus (RSV).

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Autopsies of some SIDS victims have shown pathologic changes, including smooth muscle thickening in small pulmonary arteries, right ventricular hypertrophy, hematopoiesis in the liver, increase in periadrenal brown fat, adrenal medullary hyperplasia, and abnormalities of the carotid body. Other markers reported with some regularity include brainstem gliosis and increased neuronal apoptosis in the brainstem and hippocampus. These were thought to be indicative of long-standing hypoxemia and, in the early 1990s, attention focused on an association between SIDS and sleeping in the prone position.5,6 Epidemiologic ...

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