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; Attending Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota
Contributor Information and Disclosures

Updated: Oct 1, 2009

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 one of 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

Understanding of the genetic, environmental, and biologic factors involved in the pathogenesis of SIDS continues to evolve. SIDS likely represents an interaction of factors, including (1) a vulnerable infant who possesses intrinsic abnormalities in cardiorespiratory control, (2) a critical period of development of homeostatic control mechanisms, and (3) exogenous stressors. See Triple risk model in Causes.

Leiter 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.1 Kinney notes that the defects in these critical life-sustaining neural pathways likely arise during fetal development and, in some cases, are further influenced by prenatal and postnatal exposure to cigarette smoke and alcohol.2,3

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.4,5 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 1994.6 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 has increased to 14.5% in 2008 is of some concern. Since 1992, SIDS rates have fallen approximately 58%. In 2006, the National Center for Health Statistics reported a total of 2323 SIDS deaths nationwide for a SIDS rate in the United States of 0.54 per 1000 live births.

Media file 2 depicts changes in incidence and sleep position prevalence before and after the "Back to Sleep" campaign.

Depiction of changes in sudden infant death syndr...

Depiction of changes in sudden infant death syndrome (SIDS) incidence in the United States before and after the "Back to Sleep" campaign. The line plot (secondary y-axis) depicts the combined proportion of infants placed for sleep in the supine and side-sleep positions determined by an annual federal telephone survey of infant sleep position. AAP=American Academy of Pediatrics; BTS=Back To Sleep.

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Depiction of changes in sudden infant death syndr...

Depiction of changes in sudden infant death syndrome (SIDS) incidence in the United States before and after the "Back to Sleep" campaign. The line plot (secondary y-axis) depicts the combined proportion of infants placed for sleep in the supine and side-sleep positions determined by an annual federal telephone survey of infant sleep position. AAP=American Academy of Pediatrics; BTS=Back To Sleep.


Media file 3 highlights elements of the "Back to Sleep" campaign.

Adapted from "The Changing Concept of the Sudden ...

Adapted from "The Changing Concept of the Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleep Environment, and New Variables to Consider in Reducing the Risk." 21

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Adapted from "The Changing Concept of the Sudden ...

Adapted from "The Changing Concept of the Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleep Environment, and New Variables to Consider in Reducing the Risk." 21


International

Significant changes have been observed in prevalence of SIDS worldwide. Hauck and Tanabe identified reductions in SIDS prevalence, ranging from 40% in Argentina to 83% in Ireland, with rates of decline leveling off in recent years.7 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 overall decline in SIDS rates was attributed to a change to the supine sleep position.8 They further note that, of 38 additional infant care variables studied, no other individual factor explains more than 7% of the overall decline in SIDS.9

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-fold to 5-fold elevated risk of SIDS compared with infants of mothers who do not smoke.10 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, breastfeeding, pacifier (dummy) use, infant bundling, head covering, 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 cites multiple epidemiologic studies finding that room sharing reduces SIDS risk by 50%.11 Ruys, Tappin et al, Matthews et al, and Fleming et al all identified elevated risk for SIDS among bed-sharing infants in case-control studies.12,13,14,5 The risk appeared to be greatest among infants younger than 3-4 months.

The effect of breastfeeding on risk for SIDS has varied in population-based studies. In a German infant cohort, breastfeeding reduced the risk of SIDS by approximately 50% at all ages throughout infancy.15 The authors recommended advocating breastfeeding through age 6 months in SIDS risk-reduction messages.

Recent studies from overseas centers have indicated that pacifier use may reduce the risk of SIDS.16 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 et al 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.17

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.

Head covering by bedding or bed clothing has been identified as a SIDS risk factor in multiple studies. Mitchell et al noted that infants who developed SIDS and were discovered with their heads covered with bedding or bed clothing were observed to be very sweaty and had a higher incidence and severity of thymic petechiae on autopsy, suggesting a causal association to the death.18 Blair et al noted in a systematic review of population-based age-matched controlled studies that the pooled prevalence of head covering in SIDS cases was 24.6% (95% confidence interval [CI], 22.3-27.1%) compared with 3.2% (95% CI, 2.7-3.8%) among controls.19 The population attributable risk estimated from this review (27.1%; 95% CI, 24.7-29.4%) suggests that avoidance of head covering could reduce SIDS deaths by more than a quarter.

Vennemann and colleagues re-examined SIDS risk factors following "Back to Sleep" initiatives in Germany and noted that although only 4.1% of the infants were placed prone to sleep, those infants were at a high risk of SIDS.20 Infants who were unaccustomed to sleeping prone were at very high risk, as were those who turned to prone. Bed sharing (especially for infants <13 wk), duvets, sleeping prone on a sheepskin, sleeping in the house of a friend or a relative (compared with sleeping in the parental home), and sleeping in the living room (compared with sleeping in the parental bedroom) increased the risk for sudden infant death syndrome. Pacifier use during the sleep continued to be associated with a significantly reduced risk of SIDS.

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 infant deaths (SUID).

Race

Population studies of SIDS in the United States have demonstrated consistently higher rates among black 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 black 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 black 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.22 The frequency and severity of petechiae have been noted to be similar regardless of whether infants have been discovered facedown on the sleep surface or with face up or face to the side. This finding suggests that centrally mediated airway failure, such as that seen with apnea or failed gasping rather than external airway obstruction, is likely in SIDS.23
  • Microscopic examination may reveal minor inflammatory changes within the tracheobronchial tree or signs of passive congestion of the organs. Very mild myocardial lymphocyte and macrophage infiltration with scattered necrotic cardiomyocytes may be seen in SIDS and are not considered to be pathologic.24
  • 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.25
    • 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 infant death (SUID).
  • 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.26,27 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 and Takashima noted that differences in CNS dopamine beta-hydroxylase and tryosine hydroxylase have been shown in infants with SIDS compared with control infants.28 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.29 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.30,31 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 serotonin-binding neural pathways critical to autonomic control and arousal. Autopsy-derived data and animal model studies have helped to identify key structural and functional components of these pathways and their potential relationships to SIDS.32,33,34,3
    • Weese-Mayer et al and Rand et al have described genetic polymorphisms associated with defects in components of serotonin-binding neural pathways.35,36 Polymorphisms in the serotonin transporter (5-HTT) promoter genes were identified more often in SIDS cases than in controls.37
  • 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 SUID. 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.38
    • 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 SUID. The principal non-SIDS categories of SUID 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 SUID 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 et al 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 SUID cases following a thorough death scene investigation.39 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. Shapiro-Mendoza et al notes that US infant mortality rates attributable to accidental suffocation and strangulation in bed have quadrupled since 1984 using CDC/National Center for Health Statistics data.40
    • In a study of the reclassification effect among sudden unexpected infant deaths in Minnesota, Moore et al noted that during the period in which there was a 50% decline in SIDS, a 2-fold to 3-fold increase in deaths attributed to overlay and positional asphyxia were observed, and an 8-fold increase in injury-related deaths, including those attributed to threats to the external airway, was noted.41
  • 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.
    • Approximately 25-50% of ALTEs remain unexplained following a thorough evaluation. The most common conditions associated with ALTE include apnea of infancy, gastroesophageal reflux disease, respiratory syncytial virus bronchiolitis, pertussis, sepsis and/or meningitis, and seizure. Less common causes include cardiac dysrhythmia (long QT syndrome [LQTS]), anemia, structural CNS anomaly, and cardiac or airway anomaly.
  • 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 occur as congenital LQTS or may arise as an adverse effect of certain medications. Congenital LQTS has several distinct genetic forms or may arise as a spontaneous mutation. 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 8 genes on 5 separate chromosomes have been identified to date.
    • Ackerman et al found that 2% of a SIDS cohort had one of the sodium channel mutations, SCN5A, which has been linked to sleep associated sudden death.42 Arnestad et al demonstrated in a Nordic cohort that 9.5% of cases diagnosed as SIDS possessed one of the 7 known mutations associated with LQTS.43 Otagiri et al noted 10% of SIDS cases in Japan were associated with mutations of the cardiac ion-channel genes.44 Millat et al reported LQTS genetic variants among 9.4% of French infants who died suddenly and unexpectedly.45 Half of the LQTS gene variants identified in this group were located on the SCN5A gene.
    • A long-term prospective study explored the relationship of QT interval prolongation and SIDS.46
      • 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 SUID 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 due to 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 most of the United States and in many centers worldwide, MCADD testing has been incorporated into expanded newborn metabolic screening programs. Rhead et al notes that tandem mass spectrometry blood spot screening established an incidence of MCADD of 1:14 600 (95% CI, 1:13 500 and 1:15 900) in 8.2 million newborns worldwide. Other prospective screening studies identified prevalences of 1:8930 newborns47 and 1:12,000.48
    • MCADD is an autosomal recessive disorder. 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).49 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.
    • Newborn screening for MCADD has detected cases with a wide range of genotypes and biochemical abnormalities. Although most children identified by newborn screening do well, adverse outcomes have not been entirely avoided.50
    • Defects in fatty acid beta-oxidation should be considered 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).
  • Infant homicide and SUID
    • 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. Alveolar hemosiderin-laden macrophages (HLMs) in histological sections of the lung represent evidence of previous pulmonary hemorrhage. The presence of HLMs, although not diagnostic, have been identified more often in infants who have experienced abusive trauma than in control infants.51

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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References

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Further Reading

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Keywords

sudden infant death syndrome, SIDS, crib death, cot death, sudden unexpected infant death, SUID, 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; Attending 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; Head, Division of Pulmonary Medicine; 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: Genentech Honoraria Speaking and teaching; Genentech Honoraria Consulting; Novartis Honoraria Consulting; Altus  Consulting fee Consulting; Axcan Scandi Consulting fee Consulting; Boston Scientific Consulting fee Consulting; Gilead  Speaking and teaching

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

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; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD, Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center
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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