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Sudden Infant Death Syndrome (SIDS)

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 SIDScontinues 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 inCauses.

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.1Kinney 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.4,5These 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 generalpublic that placing infants supine for sleep had the potential to significantly reduce the frequency of SIDS.

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This was followed by the official federal "Back to Sleep" campaign launched in the Spring of 1994.6This

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 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.

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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.7These 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.8They 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

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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.10The

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%.11Ruys,

Tappin et al, Matthews et al, and Fleming et al all identified elevated risk for SIDS among bed-sharing

infants in case-control studies.12,13,14,5The 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.15The

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.18Blair 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.19The 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.20Infants who were unaccustomed to sleeping prone were at very high risk, as were those who

turned to prone. Bed sharing (especially for infants

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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).

RacePopulation 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 aslow 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 (

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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 thedeath.

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.22The 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

o 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, includinga vulnerable infant possessing intrinsic abnormalities in cardiorespiratory control, a critical

period of development of homeostatic control mechanisms, and exogenous stressors.25

o Death occurs when vulnerable infants are subjected to stressors at times when normal

defense mechanisms may be structurally, functionally, and/or developmentally deficient.

o 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

o 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.26,27Reductions in the degree of myelination of specific brainregions of infants with SIDS provide further evidence of defective neuronal development.

o 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.28Abnormalities in adrenergic pathways related to cardiorespiratory control within

the medulla and pons have also been identified.

o 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 arcuatenucleus of some infants who have died of SIDS.

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including gross and microscopic dissections and the role of toxicologic, microbiologic,

radiographic, and other special procedures, are detailed by Krous (1996) and others.38

o 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-SIDScategories of SUID include infectious diseases, metabolic abnormalities, environmental

factors, and structural (congenital) cardiac, respiratory, and CNS lesions.

o 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.

o 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.39These alternative

diagnostic categories have supplanted a portion of what had previously been diagnosedas SIDS.

o 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

o 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 SIDSo Anapparent 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.

o 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 whoexperience 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.

o 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

o 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, arelationship between QT prolongation and SIDS has been the subject of much interest.

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o 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.

o 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 mayarise 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.

o 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.42Arnestad 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.43Otagiri et al noted 10% of SIDS cases in

Japan were associated with mutations of the cardiac ion-channel genes.44Millat et alreported LQTS genetic variants among 9.4% of French infants who died suddenly and

unexpectedly.45Half of the LQTS gene variants identified in this group were located on the

SCN5A gene.

o 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 developmentof 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

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varying affinities for long-, medium-, and short-chain fatty acids. Inherited defects of all 3

dehydrogenases are now recognized.

o 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 newborns47and 1:12,000.48

o 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).49Use of polymerase chain reaction (PCR) techniques

to determine the frequency of the G-985 mutation in SIDS and control populations hasfailed to demonstrate the homozygous condition in SIDS.

o 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

o 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

o 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 illnessmanifesting as Mnchausen 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.

o 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 eventreported 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 Mnchausen 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

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diagnostic, have been identified more often in infants who have experienced

abusive trauma than in control infants.51

Differential Diagnoses

Anomalous Left Coronary Artery From the PulmonaryArtery Intestinal Volvulus

Aspiration Syndromes Long QT Syndrome

Bacteremia Long-Chain Acyl CoA DehydrogenaseDeficiency

Bronchiolitis Medium-Chain Acyl-CoA DehydrogenaseDeficiency

Cardiomyopathy, Hypertrophic Meningitis, Bacterial

Child Abuse & Neglect: Physical Abuse Meningococcal Infections

Coarctation of the Aorta Myocardial Infarction in Childhood

Coronary Artery Anomalies Myocarditis, Viral

Epiglottitis Sleep Apnea

Head Trauma Ventricular Fibrillation

Hypoplastic Left Heart Syndrome

Other Problems to Be Considered

Heat injury

Tracheobronchial or esophageal foreign bodies

Bacterial, viral, and fungal sepsis

Shaken baby syndrome or nonaccidental trauma

Disorders of cardiorespiratory control

Ventricular dysrhythmias

Workup

Laboratory Studies

Establish a diagnosis of sudden infant death syndrome (SIDS) by excluding recognizable causes

of sudden unexplained infant death (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 and others.38

Imaging Studies

Obtain whole-body radiographs to evaluate for evidence of skeletal trauma. Special coned-down

radiographic views may be necessary to further delineate subtle metaphyseal corner fractures of

the long bones seen with nonaccidental forms of trauma.

Other Tests

In many jurisdictions, toxicologic screening of serum and vitreous electrolyte analysis are routinely

performed as part of the postmortem evaluation. If not routinely performed, obtain appropriatespecimens and retain them for potential analysis.

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Follow-up

Deterrence/Prevention

Sudden infant death syndrome (SIDS) risk is lowest for infants placed in the supine position for

sleep. The side-sleep position is recognized to be unstable and carries a higher risk for SIDS thanthe supine sleep position.

Recent studies from overseas centers have indicated that pacifier use may reduce the risk of

SIDS.16The pacifier may be offered to the infant when placed for sleep. Reinserting the pacifier if it

falls out is not necessary once the infant is asleep. Do not force use of the pacifier if the infant

refuses it. Clean and replace the pacifier regularly. Do not sweeten the pacifier to enhance its use.

For breastfed infants, delay pacifier introduction until the infant is older than 1 month to ensure the

establishment of breast-feeding.

Avoid overbundling and head covering, which may help reduce risk.

Avoid excessively soft or padded sleep surfaces, including pillows, comforters, and waterbeds.

Keep soft objects and loose bedding out of the crib.

Avoid cigarette smoke exposure. Create a smoke-free zone around the infant.

Although somewhat more controversial, current evidence suggests that bed-sharing should be

avoided. Bed-sharing may lead to compromise of the infants' airway, because the infant may be

suffocated by soft or loose bedding or a sleeping adult. In addition, overheating may occur.

Cosleeping on a couch or sofa is associated with an unusually high risk for SIDS and should be

avoided. The American Academy of Pediatrics (2005) recommends room-sharing as an

intervention to enhance breastfeeding but advises that once a feeding is complete, the infant

should be placed for sleep in a separate bassinet or safety-approved crib.21

Media file 4 specifies current recommendations on sleep position and the infant sleep environment

as interventions to lower the risk of SIDS.

Several key recommendations related to infant sleep position and the sleep

environment. Sources: American Academy of Pediatrics (AAP), National

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13/13

Institutes of Health and Human Development (NICHD), Consumer Product

Safety Commission (CPSC), Association of SIDS and Infant Mortality Programs

(ASIP). Adapted from "What is SIDS" monograph published by the National

Sudden Infant Death Syndrome Resource Center.

Miscellaneous

Special Concerns

In addition to notifying the medical examiner or coroner, several other key individuals should be

contacted immediately after the death.

o The infant's primary health care providers should be notified of the death so that they may

provide consolation and immediate guidance to the family. They can also provide the

infant's relevant medical history.

o If subspecialty health care providers cared for the infant, they should also be contacted for

the same reasons.

o Immediate and extended family members should be contacted to assist the family with

grief support.

o The family's religious institution and chaplain staff may also be contacted to offer

consolation and guidance to the family.

o In special cultural settings, family or tribal elders may need to be notified to assist the

family following the death.

Experts in the field of grief support describe the following strategies for supporting the family under

these difficult circumstances:

o At the time of death: Express condolences to the family. Encourage the parents and family

to see and hold the infant if they feel that they are able to do so. Explain the local

procedure that is followed after the death, including autopsy and death investigation by

local authorities. If sudden infant death syndrome (SIDS) is suggested, reassure the

family that they could not have done anything to prevent the death. Reassure the family

that intense feelings of grief are normal and that resources are available for support.

o Early support following the death (first days after death): Refer the family to the local SIDS

program (US SIDS program listings are available atAssociation of SIDS and Infant

Mortality Programs). Attend the viewing or services and send a sympathy card. Listen

supportively and allow expressions of grief. Discuss potential sibling reactions. Arrange an

appointment to discuss autopsy findings.

o Reviewing the autopsy findings: Meet with the family to discuss the results of the autopsy

and answer their questions. Discuss grief response to the loss.

o Long-term family support: Be available to families as needed. Explain that special times of

grief include the anniversaries of the infant's birth and death.

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