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I This article is the second in a three-part series reviewing recent developments in sudden infant death syndrome (SIDS) research with an emphasis on academic and clinical issues of interest to the emergency physician (EP). Part I introduced SIDS and reviewed its epidemiology and pathophysiology.' Part I1 places this material in several theoretical constructs, each proposing an etiology for SIDS that unifies all known epidemiologic and pathophysiologic features. Since current SIDS work emphasizes the role of brainstem regulation in infant cardiorespiratory and autonomic functions, this theory is expounded in detail. In addition. limitations inherent in all SIDS research that frustrate data collection and interpretation are discussed. Part I11 will offer a practical ED approach to SIDS and associated disorders. The methods used to develop this review series were described in part I of the series. ETIOLOGY OF SIDSIn addition to being consistent with present scientific knowledge and logic, a successful SlDS theory needs to: 1 ) account for all the epidemiologic and known risk factors (e.g., anatomic and pathophysiologic findings) discussed in part I; 2) explain the contradictory data derived from equally strong studies: and 3) explain why SIDS infants appear to represent a heterogeneous group. Those theories that do not fulfill the above criteria are described elsewhere. Apnea HypothesisThe apnea hypothesis has been the major SIDS theory for more than a decade. The theory is based on pathologic findings from studies of infants at risk for sudden death, epidemiologic studies. and physiologic studies of infant apnea and other respiratory abnormalities.This theory posits that some infants, for whatever reason, have recurrent episodes of abnormal ventilation, which result in both episodic alveolar hypoxia and arterial hypoxemia. Alveolar hypoxia is known to stimulate pulmonary vasoconstriction and ultimately pulmonary vascular smooth muscle hyperplasia, while arterial hypoxemia and ischemia lead to other changes, including astrogliosis of the brainstem, which promotes hypoventilation and further brainstem astrogliosis. Pulmonary vascular muscularity causes pulmonary vasoconstriction and subsequently increases right ventricular afterload. Cardiac failure results, with more severe tissue hypoxia. These two interconnected positive-feedback loops acting in concert were believed responsible for SIDS death.3 What ap-

I This article is the third in a threepart series reviewing recent developments in sudden infant death syndrome (SIDS) research with an emphasis on academic and clinical issues of interest to the emergency physician (EP). Part I introduced SIDS and reviewed its epidemiology and pathophysiology.' Part I1 reviewed how these factors have given rise to several theoretical constructs addressing an etiology for SIDS.2 Part I11 offers a practical ED approach to SIDS and associated disorders and directs attention to future areas of research and proposed interventions. Specific issues discussed include the ED identification and management of the highest-risk infants, and immediate concerns of the physician pronouncing a SIDS infant in the ED. The approach used to develop these articles is described in part I of the series.