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Bacterial infections

Definition

SIDS is a diagnosis of exclusion and should be applied to only those cases in which an infant's death is sudden and unexpected, and remains unexplained after the performance of an adequate postmortem investigation, including:

an autopsy (by an experienced pediatric pathologist, if possible);

investigation of the death scene and circumstances of the death;

exploration of the medical history of the infant and family.

 

After investigation, some of these infants deaths are found to be caused by accidental suffocation, hyperthermia or hypothermia, neglect or some other defined cause.

 

Australia and New Zealand are shifting to the term "sudden unexpected death in infancy" (SUDI) for professional, scientific and coronial clarity.

 

The term SUDI is now often used instead of sudden infant death syndrome (SIDS) because some coroners prefer to use the term 'undetermined' for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.

 

Risk factors

 

The cause of SIDS is unknown. 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 process or its potential causes. The frequency of SIDS does appear to be influenced by the infant's age or ethnicity, the education or socioeconomic status of the infant's parents.

 

Listed below are several risk factors associated with increased probability of the syndrome.

 

Prenatal

Maternal age — SIDS rates decrease with increasing maternal age, with teenage mothers at greatest risk.

Delayed or inadequate prenatal care

Exposure to nicotine from maternal smoking — SIDS rates are higher for infants of mothers who smoke during pregnancy.

 

Postnatal

Low birth weight — in the United States from 1995–98, the SIDS death rate for infants weighing 1000–1499 g was 2.89/1000; for a birth weight of 3500–3999 g, it was only 0.51/1000).

Exposure to tobacco smoke;

Prone sleeping position (lying on the stomach);

No breastfeeding;

Elevated or reduced room temperature;

Excesses of bedding, clothing, soft sleep surfaces, or stuffed animals;[22]

Anemia.[23] (note, however, that per item 6 in the list of epidemiologic characteristics below, extent of anemia cannot be evaluated at autopsy because "total hemoglobin can only be measured in living infants."[24])

Sharing a bed with parents or other siblings may increase risk for SIDS, but the mechanism remains unclear.[25]

Age of infant — SIDS incidence rises from zero at birth, is highest from two to four months of age, and declines toward zero after the infant's first year.[26]

Male sex — male children have a ~50% higher risk of SIDS than female children.[27]

Premature birth — increases risk of SIDS death roughly fourfold.[13][15] From 1995–1998 the U.S. SIDS rate for births at 37–39 weeks of gestation was 0.73/1000; the SIDS rate for births at 28–31 weeks of gestation was 2.39/1000)[15]



Mold (this hypothesis has been disproven by research subsequent to Cleveland study in the 1990's; infant pulmonary hemorrhage is most closely linked to premature birth; prematurity and water-damaged homes would both coincide with poverty)http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4909a3.htm — can cause bleeding in the lungs and a variety of other uncommon conditions that may be fatal; the presence of mold correlates positively with increased incidence of SIDS[citation needed]. Mold-related illness is often misdiagnosed as a virus, influenza, and/or an asthma-like condition.

 

Hypotheses

Bacterial infections

In a British study released May 29, 2008, researchers discovered that the common bacterial infections Staphylococcus aureus and Escherichia coli appear to be risk factors in some cases of SIDS. Both bacteria were present in greater-than-usual concentrations in infants who died from SIDS.[29] SIDS cases peak between eight and ten weeks after birth, a time when antibodies passed from mother to child are starting to disappear, but have not yet been replenished by the infant's own antibodies.

 

Bed sharing

A 2005 policy statement by the American Academy of Pediatrics (AAP) on sleep environment and the risk of SIDS deemed bed-sharing unsafe, recommending that infants sleep in a separate crib, bassinet, or cradle in the same room as a parent.[30] In 2011, the AAP issued an expansion of its recommendations for a safe infant sleeping environment, in which it again recommended "room-sharing without bed-sharing", stating that such an arrangement can decrease the risk of SIDS by up to 50%. Furthermore, it recommended against devices marketed to make bed-sharing "safe", such as in-bed co-sleepers.[31]

 

One trial compared 20 infants who shared their parents' bed one night and slept separately the next. The children's heart rate and oxygen saturation were monitored and analyzed together with eight hours of infrared video recording of their sleep. Although the bed-sharing infants spent some parts of the night with their airways (both mouth and nose) covered, "no consistent effect on either oxygen saturation levels or heart rate was revealed, even during prolonged bouts of airway covering." The authors concluded that "although numerous authors have suggested that bed-sharing infants face risks because of airway covering by bed-clothes or parental bodies, the present trial does not lend support to this hypothesis".[32]

 

Brain disorders

According to a 2006 study in the Journal of the American Medical Association (JAMA), some babies who die of SIDS have abnormalities in the brain stem (medulla oblongata) of underdeveloped serotonin receptors (which help control functions like breathing, blood pressure and arousal) and abnormalities in serotonin signaling. According to the National Institutes of Health, this finding was the strongest evidence at that time that structural differences in a specific part of the brain may contribute to the risk of SIDS.[33] This abnormality can continue postpartum until the end of the baby's first year, possibly accounting for the increased SIDS risk in premature infants and declining risk in children over 12 months of age. The authors noted that males have fewer serotonin receptors than females, perhaps contributing to the greater frequency of SIDS in males, but their follow-up 2010 paper failed to reconfirm that gender difference.[34]

 

Another 2006 study showed that a possible cause of SIDS parents leaving their infants in an angled (feet up, head down) position known as the Trendelenburg position.[35] This position can cause the brain stem to fall; in severe cases, the brain becomes "crushed". Recommended positions for resting infants include Fowler's position and Sims' position.[citation needed]

 

A 2010 study suggests Interleukin-2, a neuromodulator, as the potential mechanism of SIDS. Intense neuronal IL-2 immunoreactivity in brainstems of SIDS victims was found, which could be responsible for decreased cardiorespiratory and arousal responses.[36]

 


Date: 2015-12-17; view: 613


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