This report summarizes research on sudden infant death syndrome (SIDS). It defines SIDS as the unexpected death of an infant under 1 year of age that remains unexplained after autopsy. The report reviews SIDS rates, risk factors like prone sleeping and bed sharing, and potential mechanisms involving immature cardiorespiratory control and failure of arousal from sleep. Future directions include larger genetic studies and standardized classification to monitor trends and guide research aiming to further reduce SIDS prevalence.

1. THAT IS THE JOB
SAVING LIVES

2. MINISTRY OF HEALTH OF UKRAINE
LUGANSK STATE MEDICAL
UNIVERSITY
DEPARTMENT OF PEDIATRICSREPORT PRESENTED BY RUBEN
GOMBALANDI .
SUPERVISED BY Dr. OKSANA
BABINOVA.
ON

3. OBJECTIVE
• INTRODUCTION
• DEFINITION
• EPIDEMIOLOGY
• DEMOGRAPHIC
• PATHOPHYSIOLOGY
• AUTONOMIC CONTROL AND AROUSAL
• AUTOPSY FINDING
• NEUROANATOMICAL FINDINGS
• RISKS FACTORS
• GENE ENVIROMENT INTERACTION
• DIAGNOSIS
• PREVENTION
• MANAGEMENT AND SUPPORT
• FUTURE DIRECTIONS
• REFERENCE

4. INTRODUCTION
Sudden infant death syndrome continues to be the most common cause of
post neonatal death, account for 25% of all death between 1month of age
and 1 year of Age.
SIDS is a complex, multifactorial disorder of which the
cause is not fully understood.
Some environmental risk factors are modifiable
Reducing exposure to modifiable risk factors has lowered
the incidence of SIDS
New research indicates genetic risk factors
Actual risk of SIDS may depend on interaction of
environmental and genetic risk factors

5. DEFINITION
Sudden death of an infant under 1 year old that is
unexpected by history and unexplained after a thorough
post mortem examination

6. INVESTIGATION
Investigation includes:
Complete autopsy
Investigation of the scene of death
Review of medical history

7. EPIDEMIOLOGY
SIDS rate in United States
1990 – 1.3 per 1000 live births
2002 – 0.6 per 1000 live births
~ 3000 SIDS deaths/yr
Changes in classification of sudden unexpected deaths in
infants from SIDS to categories of asphyxia and “unknown” has
occurred in recent years
May be falsely reducing SIDS rates while overall death rate from
unexpected infant deaths remains the same

8. DEMOGRAPHY
less frequently in 1st
month of life
Peaks 2-4 month of age
90% in first 6 months of life
Boys 30-50% more likely to be affected than girls
Racial and ethnic disparities
2-3x risk for African American, Native American or
Alaska Native (irrespective of socioeconomic status)
African Americans twice as likely to place infants prone to
for sleep & twice as likely to bedshare
High rates of smoke exposure and bedsharing among
Native Americans and Alaskan Natives
Asian, South Pacific, Hispanic infants lowest incidence
Winter seasonal predominance has declined or disappeared

10. PATHOPHYSIOLOGY
Multifactorial in origin
Triple Risk Hypothesis
Vulnerable infant
Critical developmental period in homeostatic control
Exogenous stressors
Final pathway believed to involve immature cardiorespiratory and
autonomic control along with failure of arousal responsiveness from sleep

11. AUTONOMIC CONTROL AROUSAL
SIDS infants higher baseline heart rates, lower heart rate variability, prolonged
QT indexes, lower parasympathetic tone and/or high sympathovagal balance
Abnormalities of arousal
Kato and colleagues report infants who died of SIDS had fewer spontaneous
arousals from sleep and immature sleep patterns
Prone sleeping
Increases total time infants spend asleep particularly time spent in quiet
sleep, a state of reduced arousability
Also decreased spontaneous arousability, induced arousability and fewer full
cortical arousals
Associated with altered autonomic control manifest by raised heart rates,
decreased heart rate variability and increased sympathetic tone
Infants exposed to smoking in utero have decreased spontaneous and stimulus-
induced arousal from sleep

12. A GOOD NUMBER SIDS VICTIM
Child AUTONOMIC NERVOUS SYS

13. AUTOPSY FINDINGS
No pathognomonic findings
Common findings:
Petechial hemorrhages of thymus gland, visceral pleura in 68-
95%
Pulmonary congestion (89%) and edema (63%) indicative of
terminal left ventricular failure
Oronasal secretions that are typically frothy, mucoid and pink or
bloody
2/3 structural evidence of pre-existing, chronic low-grade asphyxia
Study identified increased VEGF in CSF of SIDS infants, 308
versus 85 pg/dL in controls
Hypoxia frequently precedes death in SIDS
One study of 20 SIDS infants found 50% had levels of IL-6 in CSF
equivalent to those found in infants who died of infectious diseases
Staphylococcus aureus may have role in infection as 56% of
healthy infants and 86% of SIDS infants had these bacteria in the
respiratory tract

14. NEUROANATOMICAL
FINDINGS
Structural and neurotransmitter alterations in brainstem
consistent with autonomic dysregulation
Increase in dendritic spines (marker of delayed neuronal
maturation) and delayed maturation of synapes in medullary
respiratory centers
Decreased tyrosine hydroxylase immunoreactivity in
catecholaminergic neurons
Increased number and density of 5-HT neurons with decreased
serotonin 1A and 2A receptor
 Serotonin affects various autonomic functions including
cardiorespiratory and circadian rhythms

15. MORE FINDINGS
60% SIDS cases hypoplasia of arcuate nucleus
Vital area of autonomic control and integration
Receptor abnormalities relevant to autonomic control
Decreases in binding to kainate, muscarinic cholinergic and 5-HT
receptors
Lavezzi showed alterations of the cerebellum
62% of SIDS compared to 10% controls showed neuronal
immaturity, altered apoptotic programs, negative expression
somatostatin and EN2 gene, intense c-fos expression and
astrogliosis in cortex and dentate nucleus
Water reported increased neuronal apoptosis in hippocampus
and brainstem
Neuronal loss in regions sensitive to hypoxia and regions
associated with sensation in the face

16. RISKS FACTORS

17. RISKS FACTORS DIVIDED INTO:
SOCIAL FACTORS
Increased risk with:
Lower socioeconomic
status
Younger maternal age
Lower maternal
education
Single marital status
MOTHER RELATED FACTORS
Mothers of SIDS infants:
Less prenatal care
Care initiated later in
pregnancy
Low birth weight
Preterm birth
IUGR
Shorter intervals
between pregnancies (< 18
mo)
More often 2nd
or higher
order birth child

18. SUBSTANCE USE AS A PREDISPOSING FACTOR

19. INFANT SLEEP PRACTICE AND ENVIROMENT
Prone sleeping consistently shown to increase risk of SIDS
Highest risk when usually placed in another sleeping position but
were placed on stomach for last sleep, “unaccustomed prone”, more
likely to occur outside the home such as day care centers
Also risk of choking highest in prone position
Placing infant on side still places risk twice as likely to die of SIDS
compared to sleeping supine
Exceptions may be made with certain medical conditions
Soft sleeping surfaces 2 to 3 fold increase risk of SIDS
Prone sleeping + soft bedding  20 fold increase
Overheating with increased room temperature, high body temperature,
sweating or excessive clothing increase incidence
No increase with high external environment temperature
No protective effect from bed sharing
Advocates of this practice typically promoters of breast feeding
1/3 reduction with sleeping in parent’s bedroom in separate crib

20. INFANT FEEDING PRACTICE AND
EXPOSURE
Association between breast-feeding and SIDS inconclusive
Recent study showed breast-feeding associated with decreased risk of
postneonatal deaths overall but not decreased risk of SIDS
Decreased risk with pacifier use
Not known whether direct effect or associated infant or parental behaviors
Pacifier use and dislodgement may enhance arousability
No association between pacifier use and breast-feeding duration
Small increased in otitis media, respiratory tract and GI tract illnesses
Must use consistently, one study showed increased risk of SIDS if pacifier
was not used before last sleep
AAP recommends pacifier use once breast-feeding has been
established

21. GENE ENVIROMENT INTERACTION

22. GENETICS RISK FACTORS
Sodium (SCN5A) and Potassium channel polymorphisms associated
with long QT syndrome
5-10% of SIDS cases associated with defective cardiac ion channel
with increased potential for lethal arrhythmia
Polymorphisms in serotonin transporter (5-HTT) gene
Increased in transporter activity, reducing 5-HT concentrations at nerve endings
Autonomic nervous system development genes (PHOX2A, RET, ECE1,
TLX3, EN1)
Polymorphisms in promoter of anti-inflammatory cytokine IL-10 
decreased antibody production and increased inflammatory cytokines
SIDS infants w/mild respiratory infections before death were more likely
than SIDS infants without infection and controls to have deficient
complement C4 gene (C4A, C4B)

23. DIAGNOSIS
By definition, SIDS is a diagnosis of exclusion
Protocols for standardized autopsies and death scene investigations have been
published
However, wide variability in protocols in both content and frequency with which
they are implemented across jurisdictions, within countries and across different
countries
Cause of death can be difficult to diagnose from autopsy alone
Examination of circumstances present immediately before death including detailed
description of sleep environment have been increasingly emphasized in recent years
Surveys of medical examiners and coroners have reflected how much more
complicated, confusing and time consuming SIDS case have become
Most also noted they used to label many more infant death cases as SIDS than
they do now
This may be an effect of confusing risk factors for SIDS
Reaching consensus internationally on a classification scheme is essential to accurately
monitor trends and direct future research

25. RISK REDUCTION
Campaign to reduce risk of SIDS began in 1994 in the United
States
Largely focused on reducing prone sleeping and promoting
supine positioning
Some campaigns also included messages to reduce smoking during
pregnancy
No significant changes in these behaviors and reduced SIDS rates mostly
attributed to avoidance of prone sleeping
Breast-feeding advocates have opposed discouraging bed
sharing as they worry these measures will reduce breast-
feeding frequency and duration and prevent families from
enjoying the experience and benefits of bed sharing

26. FUTURE DIRECTIONS
Despite decrease in prevalence of SIDS, more work is needed
Elucidation of risk and protective factors with appropriately targeted and
implemented interventions leading to increased adoption by families
Unlikely disorder is completely eliminated or reduced to lowest possible rates
until specific causative mechanisms are more fully understood
Need studies with larger sample sizes and infants from highest risk
groups
Investigations of still births and sudden unexplained deaths in children
over 1 year of age might provide additional insights
Surveillance of trends in rates of SIDS comparisons across jurisdictions and
internationally according to a universal, standardized classification protocol
Will require multidisciplinary and collaborative effort to understand
more

27. REFERENCE
Hunt CE, Hauck FR. Sudden infant death syndrome. Cmaj. Jun 20
2006;174(13):1861-1869.
Moon RY, Horne RS, Hauck FR. Sudden infant death syndrome. Lancet.
Nov 3 2007;370(9598):1578-1587.
Weese-Mayer DE, Ackerman MJ, Marazita ML, Berry-Kravis EM.
Sudden Infant Death Syndrome: review of implicated genetic factors. Am
J Med Genet A. Apr 15 2007;143A(8):771-788.
Gurbutt D, Gurbutt R. Risk reduction and sudden infant death
syndrome. Community Pract. Jan 2007;80(1):24-27.
Fleming P, Blair PS. Sudden Infant Death Syndrome and parental
smoking. Early Hum Dev. Nov 2007;83(11):721-725.
Damato EG. Safe sleep: can pacifiers reduce SIDS risk? Nurs Womens
Health. Feb 2007;11(1):72-76.