Can a baby survive SIDS

Quiet, eerie and mysterious

The pediatricians have the following justification for sleeping in the prone position. Since the back surface gives off less heat than the ventral surface, heat stress occurs. A duvet over your head, sinking into soft mattresses, sheepskins and sleeping in the parents' warm bed can not only hinder breathing, but also create heat stress.

 

In contrast, according to the researchers, SID risk factors such as mild febrile infections, excessive sweating, excessively high nighttime temperatures in the children's room, clothing that is too warm in bed and passive smoking can only be logically explained by heat stress. There are indications that the heat stress in infections prolongs apneas.

 

Nicotine, on the other hand, has a vasoconstrictive effect and the reduced blood flow can limit the heat dissipation. The scientists explain, for example, that increased rectal temperatures have been found in children of smokers.

 

Acquittal for vaccinations

 

The often-voiced suspicion that vaccinations increase the risk of infant death has now been dispelled. On the contrary: large studies show that control children are vaccinated significantly more often than those who have died. In an English study (6), for example, only just under half of the deceased children (149 of 309) had already received a first vaccination, compared with two thirds (822 of 1234) of the children of the same age who survived. Experts recommend the pertussis vaccination in particular, as whooping cough can pave the way for sudden infant death.

 

According to experts, the only reason why vaccinations were suspected is that the peak frequency of infant deaths coincides with the age at which infants usually receive their first vaccinations. A causal connection with vaccinations, including the six-fold vaccination, could not be proven.

 

In search of the causes

 

The definition of SID relates to the absence of a cause of death. But that's absurd because nobody dies without a cause, not even an infant. That is why many pathologists are concerned with the question: What are the causes that are difficult to detect and that have so far remained undetected in an autopsy?

 

There are many indications that breathing regulation and the wake-up reactions are disturbed in SID children. That would also explain the only consistent autopsy finding in over 90 percent of SID victims: tiny punctiform capillary bleeding on the thymus, pericardium and / or the serous skin of the two halves of the thorax. In the animal model, this bleeding can be triggered by strong fluctuations in the intrathoracic pressure with simultaneous hypoxia. Obstructions in the upper airways and / or gasping for breathing also produce these findings.

 

Recordings of children who died despite being monitored in many cases show bradycardia, presumably caused by hypoxia, followed by gasping. It remains unclear why the children do not wake up and free themselves from the hypoxia-induced situation. Because the clearly audible gasping for air usually ends completely normal short nocturnal pauses in breathing, which occur again and again in babies or adults who snore. The younger a child is, the more often these breathing pauses occur. Up to the age of three months, they become continuously rarer.

 

Disturbances in the metabolism of serotonin, which plays a decisive role in mediating the wake-up reaction, may be responsible for these deficits. At least different research teams were able to independently show that a homozygous mutation in the gene for the serotonin transporter protein is linked to the occurrence of SID.

 

British researchers also believe that the failure of the emergency program for breathing control is the cause of sudden infant death syndrome (16). They identified a group of nerve cells in the brain that give the command to gasp when there is an acute lack of oxygen. This process is regulated by a protein in the cell envelope, which acts like a sluice to regulate the influx of sodium ions. The activated nerve cells then cause the respiratory muscles to contract suddenly, so that oxygen immediately reaches the lungs. If the key protein is defective, this mechanism fails. The body cannot compensate for the lack of oxygen.

 

In principle, anything that depresses the oxygen content in the blood increases the risk of prolonged breathing pauses. The tongue is relatively large in infancy. If she falls asleep, she can sink back and partially or completely block the airway. This effect is intensified when the throat muscles relax, which is regularly the case with infections of the upper respiratory tract. This is why it is so important to use α-sympathomimetics to ensure that the baby's nasal mucous membranes do not swell too much. In the first few months of life, children breathe almost exclusively through their noses and, unlike older children, cannot automatically switch to mouth breathing. However, except in rare exceptions, an infection should not have an independent significance as a cause of death.

 

Hypotheses and speculations

 

Most scientists today have deviated from the theory of the primarily fatal respiratory regulation disorder and postulate a generalized disorder of the central nervous system as the actual cause. This then includes a disruption of the respiratory regulation.

 

This theory is based on the fact that the nervous system changes fundamentally in the first year of life, because essential functions such as breathing, wake-up reactions or temperature regulation must first mature. This process does not proceed evenly, but in batches. The child's organism only replaces old regulatory systems with more sophisticated ones when they have matured sufficiently. The transition phases between two levels, however, are times of increased risk, because the new system must first prove itself.

 

This model fits the observation that children who survived an "apparently life-threatening event" (OLD) subsequently have bradycardias that occur independently of prolonged breathing pauses. It is believed that this is an expression of a disorder in the central nervous system.

 

Scientists at the University of Padua say that a QT stretch prolongation could also be the cause of death in a third of the children affected (19). You detected a spontaneous mutation in the cardiac sodium channel gene in QT syndrome. A few years earlier, the same working group had shown in a large prospective study that a longer QT segment increases the risk of SID by a factor of 41. If the results are confirmed, prevention would be possible in at least some of the children, because a QT segment lengthening can easily be recognized in the ECG. There are also effective drugs with beta blockers. In addition, the findings suggest that more consideration should be given to screening newborns with the ECG.

 

Viruses and bacteria suspected

 

Viruses are also on the SID suspect list. A research team from Bonn discovered Coxsackie viruses and parvoviruses B19 in the heart tissue of every fifth of the 60 deceased infants examined (16). The resulting viral myocardial inflammation cannot be detected microscopically until two to three days after the infection. However, since the babies apparently die shortly after the infection, there is no intervention. Almost all children are confronted with such viruses in the first few years of life; why some show symptoms and others don't is speculation.