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Sudden Infant Death Syndrome - What you need to know

Infant and Children | August 16, 2014 | Author: The Super Pharmacist

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Sudden Infant Death Syndrome - What you need to know

Sudden infant death syndrome (SIDS) is a term that has been used since the 1970s to describe the unexpected death of an infant or young child, where subsequent investigations have failed to demonstrate a cause of death. SIDS is suspected when a previously healthy infant, usually younger than six months of age, is found dead following a period of sleep. In most cases, no sign of distress is identifiable. The baby typically feeds normally prior to going to sleep. The infant is then discovered lifeless, without pulse or respiration.

The existence of this reality creates anxiety and stress for all parents and sorrow for those who lose their children.

In 1989, an expert panel from the National Institute of Child Health and Human Development revised the definition of SIDS. The current definition is

"the sudden death of an infant less than one year of age that cannot be explained after a thorough investigation is conducted, including a complete autopsy, examination of the death scene, and review of the clinical history." 

SIDS is sometimes called "crib death" or "cot death" because it is associated with the time frame when the baby is sleeping.  Ninety percent of SIDS deaths occur in the first six months of life, with a peak age of two to four months. Boys are more likely to die of SIDS than girls. There is also a higher rate of SIDS within certain racial or ethnic groups, including Indigenous Australians, New Zealand Maoris, African Americans and Native Americans.

What Causes Sudden Infant Death Syndrome?

Although multiple hypotheses have been proposed as the pathophysiologic mechanisms responsible for SIDS, none have been proven. The triple-risk model, proposed by Filiano and Kinney, suggests that SIDS represents an intersection of factors, including the following:

  • A vulnerable infant possessing intrinsic abnormalities in cardiorespiratory control
  • A critical period in the development of cardiorespiratory control mechanisms
  • Exogenous extrinsic stressors (triggering factors such as smoke exposure, improper sleep environment, overheating)

In infants succumbing to SIDS, the final common pathway appears to involve abnormal cardiorespiratory control, specifically an inadequate/incomplete ability to arouse from sleep. 

Children dying from SIDS may have a different hypoxic gasping pattern, which is associated with ineffective auto-resuscitation (ineffective increase in heart rate and respirations) compared with otherwise healthy infants or those dying of non-SIDS causes. 

Regulation of serotonin concentration may also have an important role in determining susceptibility to SIDS.

Differences in genes regulating serotonin concentration in nerve endings have been found between infants whose deaths have been attributed to SIDS and matched, non-SIDS controls. 

Brainstem abnormalities involving the serotonergic (5-HT) system have been found in up to 70% of SIDS infants. Serotonin is important in coordinating many respiratory, arousal, and autonomic functions, and it is believed that functional serotonin is critical in the normal protective responses to stressors that commonly occur during sleep.

Changes consistent with chronic brainstem hypoxic injury have also been noted in SIDS victims, which suggests that SIDS may not always be the result of a discrete, single event but rather the culmination of multiple, subtle brainstem disturbances occurring over hours or even days. 

Research from the University of Adelaide School of Medical Sciences has determined that the presence and distribution of a protein called β-amyloid precursor protein (APP) in the brains of babies who succumb to SIDS are remarkably similar to those of children who die of accidental asphyxiation. According to the research director, Professor Roger Byard, in one case, the presence of APP staining in a baby who had died of SIDS led to the identification of a significant sleep breathing problem (apnea) in the deceased baby’s sibling. This raised the possibility of an inherited sleep apnea problem - knowledge that could save the child's life.

What Are the External/Environmental Risk Factors for SIDS?

  • Laying baby to sleep on the tummy or side (prone or side sleeping position)
  • Exposure to tobacco smoke before and after birth
  • Soft sleeping surfaces
  • Overheating/ overwrapping
  • Bed sharing, particularly with mothers who smoke, infants younger than 11 weeks, alcohol consumption, and on a couch or sofa
  • Previous SIDS death in a sibling
  • Premature or low birth weight infants
  • Not using a soother/pacifier at sleep time
  • Not breastfeeding

Why Is the Incidence of SIDS Declining?

Thanks to aggressive educational campaigns such as SIDS and Kids in Australia and Safe to Sleep® in the United States, the incidence of SIDS has declined dramatically over the last two decades. SIDS and Kids safe sleeping campaign is evidence-based information developed by researchers from across Australia and internationally. 

There are six key messages in the SIDS and Kids campaign to reduce the risk of SIDS and fatal sleep accidents:

1. Sleep baby on the back from birth, not on the tummy or side‚Äč

2. Head and face uncovered

3. Smoke free before birth and after

4. Provide a safe sleeping environment night and day

5. Sleep baby in their own safe sleeping place in the same room as an adult care-giver for the first six to twelve months

6. Breastfeed baby when possible - 

Recent well-controlled studies have consistently shown that infants who were never breast-fed were two or three times more likely to die of SIDS than their breast-fed counterparts. 

Because of its high content of immunoglobulins and other antibacterial agents, breast milk has also been shown to have protective effects against illnesses such as rotavirus infections, ear infections, and upper and lower respiratory tract infections.

It is not clear why breast-feeding is protective against SIDS

TheSafe to Sleep® campaign (developed by the U.S. Department of Health and Human Services) level A recommendations are as follows:

  • Back to sleep (supine) for every sleep
  • Use a firm sleep surface
  • Room-sharing without bed-sharing is recommended
  • Keep soft objects and loose bedding out of the crib
  • Pregnant women should receive regular prenatal care
  • Avoid smoke exposure during pregnancy and after birth
  • Avoid alcohol and illicit drug use during pregnancy and after birth
  • Breastfeeding is recommended
  • Consider offering a pacifier at nap time and bedtime
  • Avoid overheating

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References

Willinger, M., James, L. S., & Catz, C. (1991). Defining the sudden infant death syndrome (SIDS): Deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatric Pathology, 11, 677-684.

Sudden infant death syndrome. MyVMC. http://www.myvmc.com/diseases/sudden-infant-death-syndrome-sids/ Updated 19 March 2014. Accessed 8 Aug 2014.

Filiano JJ, Kinney HC. A perspective on neuropathologic findings in victims of the sudden infant death syndrome: The triple-risk model. Biol Neonate. 1994;65:194-197.

Hunt CE. The cardiorespiratory control hypothesis for sudden infant death syndrome. Clin Perinatol. 1992;19:757-771.

Sridhar S, Thach BT, Kelly DH, et al. Characterization of successful and failed autoresuscitation in human infants, including those dying of SIDS. Pediatr Pulmonol. 2003;36:113-122.

Panigrahy A, Filiano J, Sleeper LA, et al. Decreased serotonergic receptor binding in rhombic lip-derived regions of the medulla oblongata in the sudden infant death syndrome. J Neuropathol Exp Neurol. 2000;59:377-384.

Ozawa Y, Takashima S. Developmental neurotransmitter pathology in the brainstem of sudden infant death syndrome: a review and sleep position. Forensic Sci Int. 2002;130(suppl):S53-S59.

Machaalani R, Say M, Waters KA. Serotoninergic receptor 1A in the sudden infant death syndrome brainstem medulla and associations with clinical risk factors. Acta Neuropathol. 2009;117:257-265.

Kinney HC, Randall LL, Sleeper LA, et al. Serotonergic brainstem abnormalities in Northern Plains Indians with the sudden infant death syndrome. J Neuropathol Exp Neurol. 2003;62:1178-1191.

Biondo B, Magagnin S, Bruni B, et al. Glial and neuronal alterations in the nucleus tractus solitarii of sudden infant death syndrome victims. Acta Neuropathol. 2004;108:309-318.

Jensen LL, Banner J, Ulhøi, BP and Byard, RW. β-Amyloid precursor protein staining of the brain in sudden infant and early childhood death. Neuropathology and Applied Neurobiology. 2014; 40: 385–397.

New insight into SIDS deaths points to lack of oxygen.Neurosciencestuff.tumblr.com. http://neurosciencestuff.tumblr.com/post/82954877424/new-insight-into-sids-deaths-points-to-lack-of-oxygen/Published 16 April 2014. Accessed 8 Aug 2014.

Safe sleeping. sidsandkids.org http://www.sidsandkids.org/safe-sleeping/ Updated 2 July 2014. Accessed 8 Aug 2014.

Safe to Sleep®: public education campaign. National Institute of Child Health and Human Development. http://www.nichd.nih.gov/sts/about/environment/Pages/look.aspx/ Updated 23 Sept 2013. Accessed 8 Aug 2014.

Milligan RA, Pugh LC, Bronner YL, et al: Breastfeeding duration among low income women. J Midwifery Womens Health 2000; 45:246-252.

Gordon AE, Saadi AT, MacKenzie DA, et al: The protective effect of breast feeding in relation to sudden infant death syndrome (SIDS): III. Detection of IgA antibodies in human milk that bind to bacteria toxins implicated in SIDS. FEMS Immunol Med Microbiol 1999; 25:175-182.

Gordon AE, Saadi AT, MacKenzie DA, et al: The protective effect of breast feeding in relation to sudden infant death syndrome: II. The effect of human milk and infant formula preparations on binding of Clostridium perfringens to epithelial cells. FEMS Immunol Med Microbiol 1999; 25:167-173.

Ford RP, Taylor BJ, Mitchell EA, et al: Breastfeeding and the risk of sudden infant death syndrome. Int J Epidemiol 1993; 22:885-890.

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