Research
There has been a substantial reduction in the number of babies lost to sudden infant death syndrome (SIDS) or cot death as it is commonly known since 1991 and the ‘Back to Sleep’ campaign. However, in the UK alone approximately 5 babies still die unacceptably every week during the first year of their life.
Delayed Organ Development
There is considerable scientific information from around the world highlighting the risks for cot death and pointing towards an infant born with hidden developmental vulnerability. Our research has centred on how babies who die as a result of cot death grow and develop whilst in utero. We have undertaken numerous studies analysing different organs to better understand what impact delayed organ development might have on a child’s well being after birth. The findings of these studies emphasize that several organs critical for survival post birth (e.g. lungs, kidneys and certain regions of the brain) do not develop to their maximum potential. Unfortunately, it is not possible for these organs to make up for lost time after birth. It is also probable that arrested or delayed development of these organs may impact on the child’s quality of life beyond the initial post neonatal period and into adulthood.
Current Research
The organ that plays the greatest role whilst a baby is developing is the placenta or the afterbirth. This organ is responsible for the transfer of all nutrients and oxygen to the baby and the removal of waste products. Any abnormality within the placenta has the potential to adversely affect the way the baby develops.
We have analysed different subcomponents of placentae from babies who died as a result of SIDS and compared them to normal healthy control placentae using highly sophisticated microscopical techniques. Our findings show that placentae from SIDS infants develop differently from controls. In particular, the greatest differences lie in the intermediate villi of SIDS placentae; this structure has a shape that is completely different to that of control placentae. Intermediate villi with a different shape may impinge on blood flow dynamics from the mother to the baby. Additionally, there are noticeably fewer blood vessels in some SIDS placentae further compromising the delivery of nutrients to the growing baby. Our conclusion is that developmental changes in the placenta may impinge on the development of the baby and may make it more susceptible to SIDS after it is born. Since placental features develop in an orderly fashion, we can get an idea at what time point a change is likely to have occurred and also what organ(s) within the baby might be affected.
The Future
Research within the unit is at present focused on exploring specific growth factors to determine when changes in blood vessel development in SIDS placentae are likely to have taken place. Additionally, placentae from women who gave birth to babies born intra uterine growth restricted (IUGR) and who themselves suffered from pre-eclampsia during their pregnancy have also been analysed using the same technique. We have to date made considerable progress in establishing that placentae from pre-eclamptic mothers develop along diverging pathways and reflect two unique subsets within the pre-eclamptic population. Each population is associated with separate clinical problems affecting the developing baby, the mother or both. We are currently investigating what changes in placental development are responsible for initiating the maternal symptoms of pre-eclampsia.
