eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Sudden Infant Death Syndrome

Author: Patrick L Carolan, MD, Adjunct Associate Professor, Departments of Pediatrics, Family Practice, and Community Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant Death Center, Consulting Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota
Contributor Information and Disclosures

Updated: Nov 21, 2007

Introduction

Background

Sudden infant death syndrome (SIDS) is defined as the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including the performance of a complete autopsy, examination of the scene of death, and review of the clinical history.

Cases that fail to meet the standards of this definition, including those without a postmortem investigation, should not be classified as SIDS. Cases that are autopsied and carefully investigated but remain unresolved may be designated as undetermined or unexplained.

References to SIDS are noted throughout recorded history. Use of the term SIDS was adopted by an international work group in 1969. The National SIDS Act of 1974 recognized SIDS as a significant public health issue in the United States and provided funding for research and for the establishment of information and counseling programs in each of the 50 states.

SIDS is the single most common cause of death in the postneonatal period (ie, in infants aged 1 mo to 1 y). In most series, SIDS accounts for 35-55% of deaths within the postneonatal period. SIDS comprises approximately 20-25% of deaths in those younger than 1 year. Despite intensive study and advances in the understanding of associated factors, the specific cause or causes of SIDS remain unknown.

Pathophysiology

The genetic, environmental, and biologic factors involved in the pathogenesis of SIDS are becoming more clear. SIDS likely represents an intersection of factors, including a vulnerable infant who possesses intrinsic abnormalities in cardiorespiratory control, a critical period of development of homeostatic control mechanisms, and exogenous stressors. See Triple risk model in Causes. 

Leiter (2007) and others have proposed that the pathogenesis of SIDS involves a persistence of fetal reflex responses into early infancy, during which enhanced inhibitory and depressed excitatory cardiorespiratory reflex responses to local stressors are present, leading to sudden death during sleep in otherwise normal-appearing infants.

Frequency

United States

The prevalence of SIDS has changed dramatically following worldwide public health campaigns that have focused on placing infants on their backs (supine position) for sleep. The impetus for this change in sleep practice for infants evolved from population-based studies conducted in centers in Great Britain, Scandinavia, Australia, and New Zealand in the late 1980s and early 1990s.1,2 These studies demonstrated that the risk of SIDS was highest for prone (ie, tummy-down) sleeping infants, intermediate for side-sleeping infants, and lowest for infants placed supine for sleep.

  • A multiagency statement directed by officials at the National Institutes of Child Health and Human Development (NICHD) was issued in the spring of 1992. It alerted health care providers and the general public that placing infants supine for sleep had the potential to significantly reduce the frequency of SIDS. This was followed by the official federal "Back to Sleep" campaign launched in the Spring of 1994.3 This effort was jointly sponsored by the NICHD, American Academy of Pediatrics (AAP), Association of SIDS and Infant Mortality Programs (ASIP), SIDS Alliance, and the United States Public Health Service.
  • Following the "Back to Sleep" campaign, federal SIDS researchers have conducted annual surveys to examine how infant sleep practices and SIDS rates have changed. These studies, conducted by NICHD, demonstrated that the rate of prone sleeping for infants decreased from approximately 75% in 1992 to a low of 11.3% in 2002. The observation that the rate of prone sleeping increased to 13% in 2004 is of some concern. Since 1992, SIDS rates have fallen approximately 58%. In 2002, the National Center for Health Statistics reported a total of 2295 SIDS deaths nationwide for a SIDS rate in the United States of 0.51 per 1000 live births.
  • Media file 2 depicts changes in incidence and sleep position prevalence before and after the "Back to Sleep" campaign. Media file 3 highlights elements of the "Back to Sleep" campaign.

International

Significant changes have been observed in prevalence of SIDS worldwide. These changes have followed public health campaigns that emphasized the use of the supine sleep position as a simple intervention to lower an infant's risk of SIDS.

  • These campaigns began in overseas centers in the late 1980s. Subsequent studies have established that rates of prone sleeping have fallen to 2-5% in many of these countries. Illustrating the impact of this single factor, Dwyer and colleagues estimated that 70% of the recent decline in SIDS rates was attributed to a change to the supine sleep position.4
  • With a change to supine sleep for infants, cigarette smoke exposure has emerged as one of the most important potentially modifiable risk factors associated with SIDS. Studies examining maternal smoking and SIDS conducted following "Back to Sleep" campaigns demonstrated that infants of mothers who smoke have a 2- to 5-fold elevated risk of SIDS compared with infants of mothers who do not smoke.5 The adverse effects of maternal smoking are generally believed to stem principally from in utero exposure of the fetus. Despite emphasis within "Back to Sleep" campaigns on the avoidance of cigarette smoke exposure (prenatal and postnatal), little change in the rates of maternal smoking during pregnancy has occurred in most countries.
  • Other infant care practices may modify the risk of SIDS. Bed-sharing, pacifier (dummy) use, infant bundling, and temperature regulation are examples. 
    • Bed-sharing may lead to compromise of the infants' airway because the infant may be suffocated by soft, loose bedding or a sleeping adult.  
    • Cosleeping on a couch or sofa is associated with an unusually high risk for SIDS and should be avoided. 
    • Mitchell (2007) cites multiple epidemiologic studies finding that room sharing reduces SIDS risk by 50%.6
    • Ruys (2007), Tappin (2005), Matthews (2003), and Fleming (1999) all identified elevated risk for SIDS among bed-sharing infants in case-control studies.7,8,9,2  The risk appeared to be greatest among infants younger than 3-4 months.
    • Recent studies from overseas centers have indicated that pacifier use may reduce the risk of SIDS.10 Several population-based studies have shown lower rates of pacifier use in SIDS infants compared with control subjects, suggesting a protective effect. The pathophysiologic advantages conferred through pacifier use remain unknown. Franco (2004) demonstrated that pacifier use during sleep modified cardiac autonomic balance in young infants, suggesting that non-nutritive sucking may serve a role in autonomic control in infants.11
    • Advice in campaigns to reduce risk has also focused on avoiding overbundling of infants during sleep. This advice appears to be more important for prone-sleeping infants and perhaps less of a factor for infants sleeping supine.

Mortality/Morbidity

Following careful analysis of information obtained from the complete postmortem evaluation, including death scene and historic information, SIDS predominates as the single leading cause of unexpected deaths in infancy; however, alternative diagnoses are identified in as many as 15-25% of sudden unexpected deaths in infancy (SUDIs).

Race

Population studies of SIDS in the United States have demonstrated consistently higher rates among African American infants and Native American infants compared to white, Hispanic, and Asian American infants. For example, in 1997, the National Center for Health Statistics reported that 1966 deaths occurred in white infants (0.64 per 1000 live births), while 918 deaths occurred in African American infants (1.53 per 1000 live births), a rate 2.4 times greater than that seen for white infants. In 2001, the SIDS rate for African American infants remained 2.8 times that seen for white infants (1.23 vs 0.44 deaths per 1000 live births). From 1995-2001, SIDS rates among Native American and Alaskan Indian infants were 2.4-2.9 times that seen for white infants. From 1995-2001, SIDS rates in Hispanic infants in the United States were approximately one-third lower than the rates seen in white infants.

These racial differences remain unexplained but appear to be independent of other risk factors, such as low birth weight, young maternal age, or high parity. Racial variations appear to mirror that observed for infant mortality in general. At present, little is known about the basis for these observed racial and ethnic health disparities.

Sex

Despite other notable changes in SIDS epidemiology, the male-to-female ratio has remained relatively unchanged at 3:2 in most population studies.

Age

The age at which SIDS deaths occur is a unique and characteristic feature. Approximately two thirds of SIDS deaths occur in infants aged 2-4 months. Ninety percent of deaths occur in children younger than 6 months, and 95% of deaths occur in children younger than 8 months. Few deaths occur in children younger than 1 month or children older than 8 months. This unique age at death profile suggests a relationship to neurobiologic components of infant development (see Causes).

Clinical

History

  • Infants whose deaths are attributed to sudden infant death syndrome (SIDS) are typically found pulseless and apneic associated with a period of sleep.
  • A typical history is that of an infant who had been recently fed and then placed for sleep. When next checked, the infant is discovered without pulse or respiration.
  • Infants with SIDS are typically born full term without a history of significant pregnancy-related complications.
  • Approximately 12-20% of infants with SIDS are born prematurely (<37 weeks' gestation) or at low birth weight (<2500 g).
  • Before death, infants with SIDS are thought to be feeding well and gaining weight normally.
  • Generally, no outward signs of significant health-related concerns are observed.
  • Approximately 70% of infants with SIDS have a history of minor viral upper respiratory tract or GI illness in the week preceding the death; however, these illnesses are generally not marked by high fever, respiratory distress, or signs of dehydration.

Physical

  • Infants with SIDS often display a frothy blood-tinged discharge from the nose or mouth at the time of discovery.
  • Signs of livor mortis or rigor mortis are often present.
  • Care should be taken at the scene of death to examine for signs of obstruction of the external airways, accidental entrapment of the head, or other environmental factors (eg, ambient temperature, source of heating for carbon monoxide exposures) that may have contributed to the death.
  • At autopsy, the infant usually exhibits signs of normal hydration and nutrition, which is evidence of proper care.
  • No signs of obvious or occult trauma should be present.
  • Gross examination of the organs generally reveals no evidence of a congenital abnormality or acquired disease process consistent with a recognizable cause of death.
  • Krous et al noted that intrathoracic petechiae are typically present on the surfaces of the thymus, pleura, and epicardium.13
  • Microscopic examination may reveal minor inflammatory changes within the tracheobronchial tree or signs of passive congestion of the organs.
  • Histologically, the thymus and adrenal glands are normal. 

Causes

  • Triple risk model
    • The cause or causes of SIDS are likely to be multifactorial. The triple risk model, proposed by Filiano and Kinney, suggests that SIDS represents an intersection of factors, including a vulnerable infant possessing intrinsic abnormalities in cardiorespiratory control, a critical period of development of homeostatic control mechanisms, and exogenous stressors.14
    • Death occurs when vulnerable infants are subjected to stressors at times when normal defense mechanisms may be structurally, functionally, and/or developmentally deficient.
    • This model allows for the possibility of multiple potential stressors and for heterogeneity in underlying vulnerabilities that manifest as sudden unexplained death in infancy (SUDI).
  • Neuropathology and SIDS
    • Numerous structural and functional nerve cell abnormalities have been described in infants with SIDS. Evidence suggesting delayed development of the brain stem has been demonstrated in 2 studies in which elevated dendritic spine counts were noted among infants who have died of SIDS.15,16 Reductions in the degree of myelination of specific brain regions of infants with SIDS provide further evidence of defective neuronal development.
    • Several studies have demonstrated neurotransmitter abnormalities in infants with SIDS. Ozawa (2002) noted that differences in CNS dopamine beta-hydroxylase and tryosine hydroxylase have been shown in infants with SIDS compared with control infants.17 Abnormalities in adrenergic pathways related to cardiorespiratory control within the medulla and pons have also been identified.
    • Some infants with SIDS have fewer acetylcholine-binding (muscarinic) receptors within the arcuate nucleus. This nerve cell complex, which resides within the ventral surface of the medulla, is thought to be critical to the integration of cardiorespiratory and arousal responses. In a subset of infants with SIDS, the arcuate nucleus was noted to be structurally deficient. Reduced kainate binding has also been noted within the arcuate nucleus of some infants who have died of SIDS.
    • Defects in serotonin-binding neural pathways have also been identified in infants who have died of SIDS.18 These pathways have been of interest because of the role they serve in cardiorespiratory control and arousal. 
    • Defective pathways have been isolated within regions of the medulla, cerebellum, limbic system and prefrontal cortex by Kinney and others. These regions all share a common origin as anlage arising from the rhombic lip in fetal development. These neural pathways are known to be developmentally complete by the second trimester of pregnancy. These observations suggest that infants who die of SIDS are subject to adverse conditions in utero, resulting in an array of structural and neurochemical abnormalities residing within neural pathways critical to autonomic control and arousal. 
    • Weese-Mayer (2007) and Rand (2007) have described genetic polymorphisms associated with defects in components of serotonin-binding neural pathways.19
  • Critical developmental period
    • The age at which SIDS deaths occur is a unique and characteristic feature. The peak of occurrence is observed in infants aged 2-4 months. Of SIDS deaths, 90% occur in children younger than 6 months. This time frame encompasses a period of dramatic developmental change for infants involving sleep state organization, arousal, cardiorespiratory control, and metabolism.
    • During this period, a near doubling of brain weight occurs, corresponding to the rapid changes that are occurring to integrate function of brain regions that serve cardiorespiratory control and arousal. Within this context, subtle challenges conceivably offered by environmental stressors may result in sudden unexpected death among developmentally vulnerable infants.
  • Exogenous stressors
    • Precipitating stressors may vary greatly across the spectrum of SIDS cases. Stressors may include changes in the concentrations of oxygen or carbon dioxide within the sleep microenvironment, changes in ambient temperature, or other potential local factors.
    • In addition, interactions with infectious agents may occur; approximately 70% of infants with SIDS have a history of recent mild upper respiratory or GI illness in the days preceding death.
  • Establishing the diagnosis of SIDS
    • An infant who is discovered lifeless may be transported by the family or by first-response personnel to the nearest hospital emergency department. In a growing number of cases, when signs of death are obvious, the infant's death may be declared at the scene by first responders. Local medical examiner or coroner protocol should be followed in either instance. In many jurisdictions, specific infant death investigation guidelines exist and should be followed by prehospital or emergency department staff when an infant death has occurred.
    • National guidelines for infant death investigation have been developed by the United States Department of Health and Human Services Centers for Disease Control and Prevention (CDC). The Sudden Unexplained Death in Infancy Investigation and Reporting Form (SUIDIRF) is a reporting inventory that standardizes information collected at the scene of death.
    • Establish a diagnosis of SIDS by excluding recognizable causes of SUDI. The necessary data set includes information obtained from the scene of death, infant and family medical and social history, and autopsy examination. Guidelines for the autopsy examination, including gross and microscopic dissections and the role of toxicologic, microbiologic, radiographic, and other special procedures, are detailed by Krous (1996) and others.20
    • Following careful analysis of information obtained from the complete postmortem evaluation, including death scene and historic information, SIDS predominates as the single leading cause of death among unexpected deaths in infancy; however, alternative diagnoses are identified in as many as 15-25% of SUDI. The principal non-SIDS categories of SUDI include infectious diseases, metabolic abnormalities, environmental factors, and structural (congenital) cardiac, respiratory, and CNS lesions.
    • Improved death scene investigations have resulted in greater numbers of SUDI cases classified as deaths attributable to asphyxiating mechanisms. Examples of these cause of death determinations include positional asphyxia, mechanical or accidental asphyxia, and overlay, among other terms.
    • Pasquale-Styles (2007) noted that potential risk factors for asphyxia including bed sharing, witnessed overlay, wedging, strangulation, prone position, obstruction of the nose and mouth, coverage of the head by bedding, and sleeping on a couch were identified in 85% of SUDI cases following a thorough death scene investigation.21 These alternative diagnostic categories have supplanted a portion of what had previously been diagnosed as SIDS.
    • The magnitude of this reclassification effect on the overall decline of SIDS has varied somewhat by state, region, and country. Malloy has provided an estimate of this effect for infants in the United States using CDC/National Center for Health Statistics data.
  • Apparent life-threatening events and SIDS
    • An apparent life-threatening event (ALTE) is defined as an episode that is frightening to the observer and is characterized by some combination of apnea (central or obstructive), change in muscle tone (usually diminished), and choking or gagging. In some cases, the observer fears that the infant has died. Previously used terminology such as near-miss SIDS or aborted crib death should be abandoned because their use implies a possibly misleading close association between this type of spell and SIDS.
    • The estimated frequency of ALTEs among healthy term infants is 1-3%. A relationship between SIDS and ALTE may be present based on the observation that the risk of subsequent death among infants experiencing an ALTE is 1-2%. The risk of mortality increases to 4% among infants whose ALTE is associated with respiratory syncytial virus (RSV) infection. The risk of subsequent death increases to 8-10% for infants who experience ALTE during sleep or require some form of cardiopulmonary resuscitation (CPR). Among infants with SIDS, only 5% have a history of an ALTE preceding the death.
    • As many as 50% of ALTEs remain unexplained following a thorough evaluation (idiopathic or I-ALTE). The principal identifiable causes of ALTE include apnea of infancy, gastroesophageal reflux disease, respiratory syncytial virus bronchiolitis, pertussis, sepsis and/or meningitis, seizure, and pallid and/or cyanotic breath-holding spell. Less common causes include cardiac dysrhythmia (long QT syndrome [LQTS]), anemia, structural CNS anomaly, and cardiac or airway anomaly.
    • The evaluation and disposition of an infant following an ALTE is directed by the history of the event and careful physical examination. Diagnostic evaluation may include some of the following:
      • CBC count to screen for the presence of systemic viral or bacterial infection or anemia or both
      • Serum chemistry levels to assess for hypoglycemia, hyponatremia, hyperkalemia, or hypocalcemia
      • Blood gas analysis to look for evidence of acidosis or retention of carbon dioxide
      • Specific bacterial or viral cultures to look for respiratory syncytial virus or pertussis
      • ECG to look for evidence of LQTS or other dysrhythmia
      • Electroencephalogram (EEG) screening for epileptiform activity
      • Neuroimaging for structural CNS abnormalities
      • Polysomnography for sleep-based disturbances in cardiorespiratory control
    • In-hospital observation is suggested for most infants following an ALTE. Self-resolving episodes of choking or gagging associated with feedings may be observed in the outpatient setting. Documenting cardiorespiratory monitors may be considered for infants with apnea of infancy or other forms of cardiorespiratory control disorders.
  • LQTS and SIDS
    • Prolongation of the QT interval is associated with states of electrical instability of the heart predisposing to ventricular arrhythmias. Clinically, these dysrhythmias may present as syncope, seizures, or sudden cardiac death. Because of these clinical manifestations, a relationship between QT prolongation and SIDS has been the subject of much interest.
    • The QT interval measurement is heart rate dependent. It is calculated according to Bazett's formula. The QT interval, obtained from routine ECGs, has been defined by some as prolonged when the corrected QT interval (QTc) exceeds 440 milliseconds. Other clinicians believe the QTc to be prolonged when it exceeds 450-475 milliseconds.
    • Prolongation of the QT interval may be observed in LQTS or may arise as an adverse effect of certain medications. LQTS has several distinct genetic forms. An autosomal dominant form (Romano-Ward) and an autosomal recessive form (Jervell and Lange-Nielsen) are recognized. The latter is associated with sensorineural deafness. LQTS may also occur sporadically. Recently, the genes encoding ion-channel proteins regulating sodium and potassium ion flux have been described. Multiple mutations involving seven genes on 5 separate chromosomes have been identified to date.
    • Ackerman (2001) found that 2% of a SIDS cohort had one of the sodium channel mutations, SCN5A, which has been linked to sleep associated sudden death.22  Arnestad (2007) demonstrated in a Nordic cohort that 9.5% of cases diagnosed as SIDS possessed one of the 7 known mutations associated with LQTS.23   
    • A long-term prospective study explored the relationship of QT interval prolongation and SIDS.24
      • Screening ECGs were obtained on 34,442 newborns over an 18-year study period. Within this large cohort, 24 infant deaths occurred that were attributed to SIDS. Twelve of the 24 infants who died exhibited prolongation of the QT interval on their newborn ECG.
      • The authors of this study hypothesize that these deaths may have been prevented with medications (beta-blockers) known to suppress the development of the fatal arrhythmias associated with QT interval prolongation.
      • Despite controversy regarding its results and conclusions, this study challenges further investigation of developmental aspects of autonomic control of cardiac electrical conduction, particularly because many developmental changes are known to occur in autonomic controls during the period of vulnerability to SIDS (ie, in infants <6 mo).
      • Future studies will help to determine whether targeted or population-based screening for QTc prolongation among newborns is the best evidence-based strategy. At-risk groups currently include families with individuals previously known to be affected by LQTS, SIDS, or sudden, unexplained death in infancy or childhood.
  • Defects of fatty acid beta-oxidation and SIDS
    • Severe fatty change in the liver is noted at autopsy in a small proportion of SUDI cases. Fatty change within the liver may be observed in various conditions, including severe dehydration associated with an enterocolitis, systemic sepsis, or inherited metabolic disorders. Previously, as many as 10% of SIDS deaths were thought to be from definable inherited metabolic diseases.
    • In the fed state, glucose is the primary substrate for energy metabolism. In the fasted state, fat replaces glucose as a source of fuel. Long-chain fatty acids are mobilized from adipose tissue and are metabolized within the mitochondrion by progressive beta-oxidation. The first steps in the processing of fats are facilitated by acyl-CoA dehydrogenases. Three distinct acyl-CoA dehydrogenases have been identified with varying affinities for long-, medium-, and short-chain fatty acids. Inherited defects of all 3 dehydrogenases are now recognized.
    • The most common disorder of fatty acid beta-oxidation is medium-chain acyl-CoA dehydrogenase deficiency (MCADD). Affected children typically present within the first 2 years of life with altered mental status and hypoglycemia brought on by periods of reduced nutritional intake associated with acute viral respiratory or GI illnesses. Previously, as many as 25% of children affected with MCADD were estimated to have presented with sudden unexpected death. In many states, testing for MCADD has been incorporated into expanded newborn metabolic screening programs.
    • MCADD is an autosomal recessive disorder. A prospective screening of neonates identified a prevalence of 1 in 8930 newborns.25 Studies of the molecular basis for MCADD have demonstrated that in approximately 90% of those affected, the condition is caused by a single point mutation (G-985).26 Use of polymerase chain reaction (PCR) techniques to determine the frequency of the G-985 mutation in SIDS and control populations has failed to demonstrate the homozygous condition in SIDS. Nevertheless, consider defects in fatty acid beta-oxidation in instances of sudden death associated with fatty change of the liver on autopsy or in situations of SIDS with atypical features, eg, early neonatal death, death in children older than 1 year, history of SIDS within a family, and other selected factors.
  • Infant homicide and SUDI
    • Infant homicide has been estimated to account for 1-10% of all SUDI cases. In most deaths attributed to SIDS, no history of child abuse, neglect, or parental psychiatric illness manifesting as Münchausen syndrome by proxy is present; however, case reports or case series of infant homicide highlight the need for a thorough and competent death investigation that must include an evaluation of the infant and family medical history and review of the scene of death to accurately distinguish natural from nonnatural infant deaths.
    • Several features have been identified that may aid in distinguishing nonnatural from natural deaths.
      • In a study of 81 covert nonnatural infant deaths, 77% of the infants had a history of an ALTE manifesting as apnea, cyanosis, marked pallor, loss of muscle tone, or seizure; 48% had been hospitalized within the week preceding the death.
      • Most infants in this group had been briefly admitted because of an unusual event reported by the caregiver, but upon examination and observation, they appeared healthy. Within the hospitalized group, 19% were discharged in the morning and subsequently died at home that evening.
      • Evidence of either somatization disorder or Münchausen syndrome was present in 48% of the perpetrators. At autopsy, 43% of the infants were found with frank blood within or around the nose or mouth, as opposed to the common serosanguineous discharge that may be present in SIDS. Unusual bruises or petechiae on the face or neck were observed in 14% of the nonnatural deaths.

More on Sudden Infant Death Syndrome

Overview: Sudden Infant Death Syndrome
Differential Diagnoses & Workup: Sudden Infant Death Syndrome
Follow-up: Sudden Infant Death Syndrome
Multimedia: Sudden Infant Death Syndrome
References
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Further Reading

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Keywords

sudden infant death syndrome, SIDS, crib death, cot death, sudden unexpected death in infancy, sudden unexplained death in infancy, SUDI, upper respiratory tract illness, livor mortis, rigor mortis, intrathoracic petechiae, neurotransmitter abnormalities, delayed development of the brain stem, positional asphyxia, mechanical asphyxia, accidental asphyxia, overlay, bed sharing, apnea, apparent life-threatening event, ALTE, near-miss SIDS, aborted crib death, respiratory syncytial virus infection, RSV, gastroesophageal reflux disease, respiratory syncytial virus bronchiolitis, pertussis, sepsis, meningitis, cyanotic breath-holding spell, cardiac dysrhythmia, long QT syndrome, anemia, structural CNS anomaly, airway anomaly, hypoglycemia, hyponatremia, hyperkalemia, hypocalcemia, severe dehydration, enterocolitis, systemic sepsis, inherited metabolic disorders, medium-chain acyl-CoA dehydrogenase deficiency, MCADD

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Contributor Information and Disclosures

Author

Patrick L Carolan, MD, Adjunct Associate Professor, Departments of Pediatrics, Family Practice, and Community Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant Death Center, Consulting Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota
Patrick L Carolan, MD is a member of the following medical societies: American Academy of Pediatrics and International Society of SIDS Researchers
Disclosure: Nothing to disclose.

Medical Editor

Susanna A McColley, MD, Director of Cystic Fibrosis Center, Divisions of Pediatric Pulmonary and Critical Care, Associate Professor, Department of Pediatrics, Children's Memorial Medical Center of Chicago, Northwestern University
Susanna A McColley, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Sleep Disorders Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Nothing to disclose.

Managing Editor

Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD, Attending Physician, Pediatric Pulmonary Medicine, Columbia University Medical Center; Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

 
 
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