2. MINISTRY OF HEALTH OF UKRAINE
LUGANSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF PEDIATRICS
REPORT PRESENTED BY RUBEN
GOMBALANDI .
SUPERVISED BY Dr. OKSANA BABINOVA.
ON
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
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
9.
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
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
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
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
24.
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.