Sudden infant death syndrome

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Sudden infant death syndrome
Classification and external resources
ICD-10 R95.
ICD-9 798
OMIM 272120
DiseasesDB 12633
eMedicine emerg/407  ped/2171
MeSH D013398

Sudden infant death syndrome (SIDS) is a syndrome marked by the symptoms of sudden and unexplained death of an apparently healthy infant aged one month to one year. The term cot death is often used in the United Kingdom, Ireland, Australia, India and New Zealand, and is termed crib death in the United States.

Contents

[edit] Overview

Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.[1]

SIDS is a diagnosis of exclusion. It can only be applied to an infant whose death is sudden and unexpected, and remains unexplained after the performance of an adequate postmortem investigation including

  1. an autopsy;
  2. investigation of the scene and circumstances of the death;
  3. exploration of the medical history of the infant and family.

SIDS is responsible for roughly 1 death per 2,000 births in the U.S. It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age.

SIDS deaths in the U.S. decreased from 4,895 in 1992 to 2,247 in 2004.[2] But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%.[2] According to Dr. John Kattwinkel, chairman of the Center for Disease Control (CDC) Special Task Force on SIDS "A lot of us are concerned that the rate (of SIDS) isn't decreasing significantly, but that a lot of it is just code shifting”.[2]

[edit] SIDS Back To Sleep Campaign: History and Theory

In 1987 the Netherlands started a campaign advising parents to place their newborn infants to sleep on their backs (supine position) instead of their stomachs (prone position).[3] This was followed by infant supine sleep position campaigns in the United Kingdom, New Zealand, and Australia in 1991, the U.S. and Sweden in 1992, and Canada in 1993.[3][4]

This advice was based on physiological evidence which shows that infants who sleep on their back have lower arousal thresholds and less Slow-Wave Sleep (SWS) compared to infants who sleep on their stomachs.[5] In human infants sleep develops rapidly during early development. This development includes an increase in non-rapid eye movement sleep (NREM sleep) which is also called Quiet Sleep (QS) during the first 12 months of life in association with a decrease in rapid eye movement sleep (REM sleep) which is also known as Active Sleep (AS)[6].[7][8] In addition, slow wave sleep (SWS) which consists of Stage 3 and Stage 4 NREM sleep appears at 2 months of age.[9][10][11][12] and it is theorized that some infants have a brain-stem defect which increases their risk of being unable to arouse from SWS (also called Deep Sleep) and therefore have an increased risk of SIDS due to their increased inability to arouse from SWS.[5] In a currently used model that explains the process in which slow wave sleep is involved in memory consolidation the hippocampus acts as a temporary storage facility for new memories which are then transferred to the neocortex during slow wave sleep (SWS).[13]

Studies have shown that preterm infants,[14][15] full-term infants,[16][17] and older infants [18] have greater time periods of quiet sleep and also decreased time awake when they are positioned to sleep on their stomachs. In both human infants and rats, arousal thresholds have been shown to be at higher levels in the Electroencephalography (EEG) during Slow-wave sleep[19].[20][21]

In 1992,[22] a SIDS risk reduction strategy based upon lowering arousal thresholds during SWS was implemented by the American Academy of Pediatrics (AAP) which began recommending that healthy infants be positioned to sleep on their back (supine position) or side (lateral position), instead of their stomach (prone position), when being placed down for sleep. In 1994,[23] a number of organizations in the United States combined to further communicate these non-prone sleep position recommendations and this became formally known as the “Back To Sleep” campaign. In 1996,[24] the AAP further refined its sleep position recommendation by stating that infants should only be placed to sleep in the supine position and not in the prone or lateral positions.

In 1992, the first National Infant Sleep Position (NISP) Household Survey[25] was conducted to determine the usual position in which U.S. mothers placed their babies to sleep: (1) Lateral (side); (2) Prone (stomach); (3) Supine (back); (4) Other; (5) No Usual Position. According to the 1992 NISP survey, 13.0% of U.S. infants were positioned in the supine position for sleep.[26] According to the 2006 NISP survey 75.7% of infants were positioned in the supine position to sleep.[27]

Since 1998 there have been several studies published which report that infants placed to sleep in the supine position lag in motor skills, social skills, and cognitive ability development when compared to infants who sleep in the prone position.[28][29] In the 1998 article entitled “Effects of Sleep Position on Infant Motor Development.” [14][29] by Davis, Moon, Sachs, and Ottolini, the authors state “We found that sleep position significantly impacts early motor development.” The prone (stomach) sleeping infants in this study slept an average of 225.2 hours (8.3%) more in their first 6 months of life than the supine (back) sleeping infants.

In the 1998 article entitled “Does the Supine Sleeping Position Have Any Adverse Effects on the Child? II. Development in the First 18 Months”[30] by Dewey, Fleming, Golding, and the ALSPAC Study Team the objective of the study was “To assess whether the recommendations that infants sleep supine could have adverse consequences on their motor and mental development.” They used the Denver Developmental Screening Test (DDST) and studied infants at 6 and 18 months. According to the study, at 6 months of age, the infants who were placed to sleep in the prone position had statistically significant higher social skills scores, gross motor scores, and total development scores than those infants who were put to sleep in the supine position. In addition, the total development scores of prone sleeping infants were still higher than supine sleeping infants at 18 months of age but were no longer statistically significant. In the 2005 article entitled “Influence of supine sleep positioning on early motor milestone acquisition”[28] by Majnemer and Barr they used the Alberta Infant Motor Scale Scores (AIMS Scores) to analyze the impact of infant sleep position. They reported that “Typically developing infants who were sleep-positioned in supine had delayed motor development by age 6 months, and this was significantly associated with limited exposure to awake prone positioning.” But, the authors also note that awake prone (stomach) positioning is associated with prone (stomach) sleeping. No studies have been conducted which compare supine sleeping infants who have regular awake prone positioning (tummy time) to prone sleeping infants who have regular awake prone positioning (tummy time).

Placing infants on their stomachs while they are awake (tummy time) has been recommended to offset the motor skills delays associated with the back sleep position[28] but positioning the infant on their stomach while awake will not impact the amount of slow wave sleep[14][15][16][17][18] since tummy time only occurs when an infant is awake.

[edit] Undiagnosed conditions

Some conditions that may be undiagnosed and thus result in a diagnosis of SIDS include

[edit] Risk factors

Very little is certain about the possible causes of SIDS, and there is no proven method for prevention. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome's biological cause or causes. The frequency of SIDS appears to be a strong function of infant sex and the age, ethnicity, and the education and socio-economic status of the parents.

According to a study published in October 2007 in the Journal of the American Medical Association, babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata), which helps control functions like breathing, blood pressure and arousal. Researchers examined the medullae of 31 babies who had died of SIDS and 10 who had died from other causes. Compared to babies who died of other causes, the SIDS babies had over twice as many serotonin-releasing neurons originating in the medulla, but fewer serotonin binding sites. They also found abnormalities that appear to affect the ability to use and recycle serotonin, which is responsible for regulating mood as well as vital body functions. According to the National Institutes of Health, which funded the study, this finding is the strongest evidence to date that structural differences in a specific part of the brain may contribute to the risk of SIDS.[31]

In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be the cause of some cases of Sudden Infant Death Syndrome. Both bacteria were present at greater than usual concentrations in infants who died from SIDS.[32] SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.

Listed below are several factors associated with increased probability of the syndrome based on information available prior to this recent study.

[edit] Prenatal risks

[edit] Post-natal risks

Mold hidden in the dwelling walls, carpets, washroom, can cause Bleeding Lungs plus a variety of other uncommon conditions leading to a misdiagnoses and death. It is often misdiagnosed as a Virus, Flu, and/or Asthma like conditions. A study done in the mid 80's found that 1/3 of dwellings in America, and other countries, have some type of hidden mold.

  • low birth weight (especially less than 1.5 kg (~3.3 lb))[citation needed]
  • exposure to tobacco smoke[35]
  • prone sleep position (lying on the stomach, see sleep positioning below)[36]
  • not breastfeeding[37]
  • elevated room temperature[38]
  • excess bedding, clothing, soft sleep surface and stuffed animals[39]
  • infant's age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)[citation needed]
  • premature birth (increases risk of SIDS death by 50 times)[citation needed]

[edit] Risk reduction for SIDS

Though SIDS cannot be prevented, parents of infants are encouraged to take several precautions in order to reduce the likelihood of SIDS.

[edit] Environment

[edit] Sleep positioning

Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases "Back To Bed" and "Back to Sleep." The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the US and New Zealand.[40] However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already low in the US.[citation needed]

Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their bedding—the brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react "normally" by moving away from the pooled CO2, and thus smother. Another theory[citation needed] is that babies sleep more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants.

Arguments against infant back-sleeping include concerns that an infant could choke on fluids it brings up.[41] Hospital staff commonly place newborns on their side, although they advise parents to place their infants on their backs after going home from the hospital.[citation needed]

Other concerns raised about the Back to Sleep Campaign have included the possible increased risk of positional facial and head deformities (see positional plagiocephaly),[41] possible interference with development of good sleep habits (which in turn may have other bad effects),[41] and possible interference with motor skills development (as infants delay attempts to lift their heads, crawl, etc.).[41]

[edit] Breastfeeding

A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had 1/5 the rate of SIDS compared with non-breastfed infants, but that "it became nonsignificant in the multivariate model that included the other environmental factors". These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective."[42]

[edit] Co-sleeping

 The neutrality of this section is disputed. Please see the discussion on the talk page. Please do not remove this message until the dispute is resolved. (September 2008)

One approach to lowering SIDS rates is limiting co-sleeping. A 2005 policy statement by the American Academy of Pediatrics on sleep environment and the risk of SIDS found co-sleeping and bed sharing to be unsafe.[43] However, some data[44] has suggested that almost all SIDS deaths in adult beds occur when other prevention methods, such as placing infants on their backs, are not used. Co-sleeping studied in the West has been present mostly in poorer families where other risk factors are present.[45] while co-sleeping in other cultures such as in China is more prevalent and is done in combination with practices such as sleeping children on their back, correlating with a significantly lower rate of SIDS than the West.[46] There are also evolutionary theories as to why co-sleeping would be healthier for infants than sleeping alone.[45] Further studies have suggested that factors associated with safe co-sleeping such as enhanced infant arousals are responsible for a positive contribution to SIDS prevention.[47] Co-sleeping is made safer with the use of a bedside "co-sleeper", rather than having the infant sleep in your bed. Adult beds are unsafe for infants. The safest place for infants to sleep is a place with bedding made specifically for infants.

[edit] Secondhand smoke reduction

According to the U.S. Surgeon General’s Report, secondhand smoke is connected to SIDS.[48] Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their lungs than those who die from other causes. Infants exposed to secondhand smoke after birth are also at a greater risk of SIDS. Parents who smoke can significantly reduce their children's risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free.

The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.[49]

[edit] Sleeping area

[edit] Bedding

To prevent SIDS, many families use firm mattresses with tight-fitting sheets in cribs or bassinets. The families do not allow pillows, stuffed animals, or fluffy bedding in the cribs. In cold weather, the families dress the infants warmly in well-fitted clothing.[50]

Infants' blankets should also not be placed over their heads. It has been recommended that the infants are only covered up to their chest with their arms exposed. This will help eliminate the chances of the infant moving the blanket over their head.

[edit] Sleep sacks

In colder environments where bedding is required to maintain a baby's body temperature, the use of a "baby sleep bag" or "sleep sack" is becoming more popular. This is a soft bag with holes for the baby's arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998[51] has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study "The use of a sleeping-sack should be particularly promoted for infants with a low birth weight." The AAP also recommends them as a type of bedding that warms the baby without covering its head.[52]

[edit] Pacifiers

According to a 2005 meta-analysis, most studies favor pacifier use.[53] According to the American Academy of Pediatrics (AAP), pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear.[54] SIDS experts and policy makers haven't recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated to pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species.[54]

A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambiental factors, and it reduced the effect of other risk factors.[55] It has been speculated that the raised surface of the pacifier holds the infant's face away from the mattress, reducing the risk of suffocation. If a postmortem investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS.

[edit] Air circulation with fan use

According to a study of nearly 500 babies published the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments.[56] Author De-Kun li said that "the baby's sleeping environment really matters" and that "this seems to suggest that by improving room ventilation we can further reduce risk."[57]

[edit] Bumper pads

Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government's health department, issued an advisory[58] recommending against the use of bumper pads, stating:

The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.

[edit] Speculated associations

A number of theoretical causes have been proposed as a trigger for SIDS, but many of them are unproven or have not been thoroughly studied and peer-reviewed.

[edit] Mattress bugs

A 2002 study hypothesized that bugs feeding on baby vomit and dust could be fatal for small children, creating 'supertoxins' which spur the baby's body into overreacting, leading to anaphylactic shock.[59]

[edit] Brain disorder

 This article includes a list of references or external links, but its sources remain unclear because it lacks inline citations. Please improve this article by introducing more precise citations where appropriate. (October 2008)

A recently published research article in the Journal of the American Medical Association showed evidence that cells in the brainstem fail to develop receptors for Serotonin in the womb. This abnormality continues until after birth, supposedly until the end of their first year. This would account for there being few to no SIDS deaths after the first year of infancy and the reason the risk is more for premature infants. The SIDS Alliance/First Candle has posted a message about this along with a link to the abstract on their website (www.firstcandle.com), which can be accessed from the front page

[edit] Vitamin C

According to a 1993 article in Journal of Orthomolecular Medicine, Australian medical doctor Archie Kalokerinos performed research showing that high doses of vitamin C eliminates SIDS.[60] As SIDS was shown to be caused solely by vitamin deficiency, the article stated that it was no longer a syndrome, and that the proper disease name is now SID. As of January 2007, the Journal of Orthomolecular Medicine was not included among journals selected by the U.S. National Library of Medicine for inclusion in their Medline database.[61][62]

[edit] Toxic gases

In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.

A major plank in this explanation is the widely-observed phenomenon that the risk of cot death rises from one sibling to the next. Richardson claims that the cause is that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair[63] references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.

In 1994, the New Zealand government, under the advice of Dr. Jim Sprott, issued advice recommending new parents to either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Dr. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.[64]

However, a final report of The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis, published in May 1998, concluded that "there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants."[65] The report also states that "in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses" and "babies have also been found to die on wrapped mattresses." Dr. Sprott's website, however, claims[66][67] that the study does not actually refute his theory:

Contrary to media publicity, the 1998 UK Limerick Report did not disprove the toxic gas theory—as a highly qualified environmental scientist has stated in the New Zealand Medical Journal. In fact, the Limerick Committee's experiments proved the fungal generation of toxic gases (forms of stibine and arsine) from cot mattress materials.

According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:

In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.[68]

[edit] Central Respiratory Pattern Deficiency

There is ongoing research in the pediatric/neonatal community that has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Bötzinger complex.[69] It is possible that irregularities in neurotransmitter release (such as GABA, adenosine, and NMDA) or deficiencies in their associated receptors (including both GABAA, GABAB subtypes and NMDA-glutamate receptors) are linked to incomplete prenatal development as is evident in pre-term infants.

Genetic factors are also being studied with several rat and mouse knockouts.

[edit] Upper cervical spinal cord injury as a result of birth trauma

During birth, if the infant's head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury.[70] When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe. This is hypothesised to aggravate and prolong the spinal cord injury sustained during birth, preventing proper healing and ultimately leading to fatal breathing difficulty.

[edit] Gender

There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61.[71][72] The X-linkage hypotheses for SIDS and the male excess in infant mortality have shown that the 50% male excess could be caused by a dominant X-linked allele that occurs with a frequency of ⅓ that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of ⅔ and an unprotected XX female would occur with a frequency of 4⁄9. The ratio of ⅔ to 4⁄9 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS.

Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence is found by examination of other causes of infant respiratory death, such as inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS. See the data found at http://wonder.cdc.gov for 9ICD 911 and 912 death rates by sex.

The study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys "had significantly fewer serotonin binding sites than girls".

[edit] Child abuse

Several instances of infanticide have been uncovered where the diagnosis was originally SIDS.[73][74] This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides.[75][76][77][78] In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

The misdiagnosis of infanticide as SIDS "happens all over," Ms. Talan, a medical reporter at Newsday, said. "A lot of doctors and police don't know how to handle it. They don't take it as seriously as they should." As a result of the book's revelations, people are starting to scrutinize possible cases of this "perfect crime," which involves no physical evidence and no witnesses.[79]

British former pediatrician Roy Meadow believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent displaying Munchausen Syndrome by Proxy (a condition which he was first to describe, in 1977). During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of murder, to varying degrees on the basis of Meadow's opinion. In 2003 a number of high-profile acquittals brought Meadow's theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned.

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.[80]

[edit] Nitrogen dioxide

A 2005 study by researchers at the University of California, San Diego found that "SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life."[81] While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.

[edit] Vaccination

According to the CDC's page on SIDS and vaccines:

From 2 to 4 months old, babies begin their primary course of vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.[82]

[edit] Inner ear damage

Records of hearing tests administered to certain infants show that those who later died of SIDS had a unique pattern of partial hearing loss, according to the journal Early Human Development.[83] One suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (from other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the "line of fire" for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.[citation needed]

[edit] Side effects of SIDS risk reduction recommendations

Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the U.S. have stated that they believe that the American Academy of Pediatrics' recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.[84]

According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed.[30] Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.[85]

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis.[86] Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated "I do not think it is a medical problem—it is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense."[87] A research study on children with plagiocephaly found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.[88]

Because of the delays caused by back sleep some medical professionals have suggested that the "normal" ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider "normal" children who previously were considered developmentally delayed.[89]

Additional studies have found the following negative conditions that the back sleep position has been reported to be associated with are: Increase in Sleep Apnea, Decrease in Sleep Duration, Strabismus, Social Skills Delays, deformational plagiocephaly, and Temporomandibular Jaw Difficulties.[86] In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with Gross Motor Milestone Delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills.[90][91] In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic.[3] In addition, prior to the “Back to Sleep” campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position.[92] Supine sleeping infants cannot self-treat their own torticollis.

[edit] Further reading

  • Joan Hodgman; Toke Hoppenbrouwers (2004). SIDS. Calabasas, Calif: Monte Nido Press. ISBN 0-9742663-0-2. [93]

[edit] Notes

  1. ^ Health Canada SIDS Healthy Babies SIDS Page.
  2. ^ a b c Bowman L, Hargrove T. Exposing Sudden Infant Death In America. Scripps Howard News Service. http://dailycamera.com/news/2007/oct/08/saving-babies-exposing-sudden-infant-death-in/
  3. ^ a b c Högberg U, Bergström E (April 2000). "Suffocated prone: the iatrogenic tragedy of SIDS". Am J Public Health 90 (4): 527–31. doi:10.2105/AJPH.90.4.527. PMID 10754964. PMC: 1446204. http://www.ajph.org/cgi/pmidlookup?view=long&pmid=10754964. 
  4. ^ Rusen ID, Liu S, Sauve R, Joseph KS, Kramer MS (2004). "Sudden infant death syndrome in Canada: trends in rates and risk factors, 1985–1998". Chronic Dis Can 25 (1): 1–6. PMID 15298482. 
  5. ^ a b Kattwinkel J, Hauck F.R., Moon R.Y., Malloy M and Willinger M Infant Death Syndrome: In Reply, Bed Sharing With Unimpaired Parents Is Not an Important Risk for Sudden\Pediatrics 2006;117;994-996
  6. ^ Louis J, Cannard C, Bastuji H, Challamel MJ (May 1997). "Sleep ontogenesis revisited: a longitudinal 24-hour home polygraphic study on 15 normal infants during the first two years of life". Sleep 20 (5): 323–33. PMID 9381053. 
  7. ^ Navelet Y, Benoit O, Bouard G (July 1982). "Nocturnal sleep organization during the first months of life". Electroencephalogr Clin Neurophysiol 54 (1): 71–8. doi:10.1016/0013-4694(82)90233-4. PMID 6177520. 
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