Dove,

The fire effluent toxicology equation presents an acidosis factor in the ISO 13344:e2015 document, also found in McKenna ST, et al., Chemosphere 2018;196:429–39. https://doi.org/10.1016/j.chemosphere.2017.12.017.

A = [CO2] x 0.05 = acidosis factor

An acidosis component is also necessary for the experimental model of LQTS: Makielski JC., J Clin Invest 2006;116:297–9. https://doi.org/10.1172/JCI27689.

There is some evidence to suggest that acidosis may play a role in sudden infant death syndrome (SIDS), although it is not always present or consistently observed in cases of SIDS.

Acidosis refers to a condition in which the pH of the blood becomes too low, indicating an excess of acid in the body. Some studies have found that infants who died from SIDS had lower pH levels in their blood than infants who died from other causes, suggesting the presence of acidosis. However, other studies have not found this association.

It is important to note that SIDS is a complex and multifactorial condition that is likely caused by a combination of factors, including abnormalities in brainstem function, respiratory control, and cardiovascular regulation. While acidosis may contribute to SIDS in some cases, it is unlikely to be the sole cause of the condition.

Sorry about pulling from my Reference Database without any explanations.

With respect to the Chemosphere toxicity equation that acidosis is an additive component of... Acidosis is a toxic component of that greater equation.

You are asking, "What does a fire-effluent equation have to do with SIDS?"

Both deal with the modulating affect hypercapnia and hypoxia have on other gaseous toxins. Acidosis originates from the CO2 levels in the atmosphere around the infant.

So, you say, "What about the LQTS and SIDS?"

A longitudinal study performed in Italy found that 3 to 4 day old neonates that had a prolonged QTc, had an OR of 41.3, of later succumbing to SIDS.

SIDS is multifactorial as described by Filiano and Kinney (1994).

Yes, agreed Paul. Thank you for your reply. I hypothesize hypercapnea (respiratory acidosis) combined with metabolic acidosis and hypokalemia cause significant diaphragmatic hyper excitability in SIDS leading to diaphragmatic spasm (tetanic like contracture) and sudden respiratory arrest. With the accessory respiratory muscles working in isolation but unable to overcome pulmonary compliance (bc they’re not trained like they are say in progressive neuropathy or myopathy), the negative intrathoracic pressures generated could explain the characteristic petechiae seen at autopsy (Tardieu spots).

Proving this could easily be accomplished in an animal research lab. I just wish I could get in touch with one.

Dov Gebien MD, MSc (pathology)

DM me Dov and I can give you the name of a CRO that does animal testing. A tetanic diaphragm would only be one aspect of SIDS. It may though fill in one of the puzzle pieces to the multifactorial picture.

The SIDS question is not high on anyone’s radar currently. Physician readers don’t want to hear anymore about it.

I think “acute diaphragmatic spasm” (tetanic like contraction) would effectively paralyze this obligatory respiratory pump muscle and cause death if immediate airway interventions aren’t instituted. It would leave little to no traces at autopsy. Sadly, it appears diaphragmatic histology is either not examined for contraction band, coagulative necrosis or done at all in SIDS and other causes of sudden, unexpected death. It appears Pathologists worldwide have missed this. Pls see linked article by Kariks on diaphragmatic histology in SIDS. Article Diaphragmatic muscle fibre necrosis in SIDS