Introduction:
In this article, an attempt is made to provide a theoretical chemical reaction framework to model the famous medical mystery of Gloria Ramirez’s emergency room visit that resulted in the emergency room healthcare workers who treated the subject, experiencing acute poisoning symptoms.
Background:
The key to understanding this newly updated theoretical model is heavily dependent on the prior body of research on this medical incident.
Those prior works have pinpointed Dimethyl Sulfoxide (DMSO) and its oxidation product Dimethyl Sulfate (DMS) as the possible chemical agents responsible for those acute poisoning symptoms reported by the emergency room healthcare workers.
This updated chemical model is intended to fill-in the gaps left by the original toxicology theory that proposed the DMS formation through a poorly characterized oxidation pathway.
The organosulfur molecule DMSO is a relatively harmless and highly chemically stable substance. It is very commonly used as a pharmaceutical ingredient. It is present in items such as over-the-counter (OTC) pain relief medications and alternative medicine formulations.
It should be noted that normally individuals may not be aware of the presence of DMSO in medications that they are using due to its relative ubiquity and its largely unregulated nature, which clearly explains why at the time of investigations into the events related to the subject’s emergency room visit, the subject’s family refused any prior knowledge of DMSO as one of the pharmacological agents used by the subject.
One of the key physical properties of DMSO is its characteristic garlic like odor. It was clearly established in the prior investigations related to this case that the subject had dermally applied copious amounts of DMSO prior to that fateful emergency room visit.
The emergency room healthcare workers at the time also detected an oily sheen and a garlic like odor when they opened up her shirt to apply the defibrillator, when the person experienced severe cardiac dysrhythmia while admitted to the emergency room.
In the prior studies it was hypothesized that the purported mechanism for poisoning of the emergency room workers that lead to the development of their rapidly progressive, acute symptoms; were due to the oxidation reaction of DMSO to DMS.
But, the key missing piece in that theory was the exact chemical mechanisms responsible for that oxidation reaction. Since the oxidation reaction of DMSO to DMS is mostly possible at high temperatures in excess of 300 degree Celsius, the previous theory of DMS as the source of poisoning did not have a strong chemical footing for addressing the exact nature of the origins of DMS.
Methodology:
A new modeling that incorporated the thermal and electrochemical effects of the defibrillators was developed to understand the possible decomposition pathways for DMSO.
This new composite chemical model can successfully explain with relatively simplicity, the precise chemical reasons for the generation of noxious DMS vapors from DMSO.
Defibrillators are well known to occasionally cause burn injuries due to the thermal effects of discharging high voltage DC current on the human body.
On that eventful day, when the defibrillator was applied on the subject; in an attempt to normalize the individual’s cardiac dysrhythmia; a small portion of the DMSO that was present in copious amounts on the subject’s skin underwent immediate oxidation to DMS facilitated by a highly localized defibrillator associated thermal effect.
It should be noted that the precise area of these thermal runways associated with defibrillator discharges are difficult to determine and they do not necessarily appear in the areas surrounding the defibrillator paddles or electrodes being applied, which could explain why this thermal event was ignored or unreported during the otherwise meticulous autopsy that followed.
A possible mechanism for these defibrillator associated burns is the sudden electrostatic discharge of the electric charge that got accumulated as a result of the application of the defibrillator. Most common areas where these burn injuries occur in subjects that undergo defibrillation are in their upper and lower extremities.
This could also explain why some emergency room healthcare workers present in that room developed more severe symptoms than others. If the healthcare workers were situated closer to the body part of the subject that suffered the rapid electrostatic discharge of the accumulated electrical charge from the defibrillator, those individuals were at a greater risk of exposure to the oxidation products of DMSO.
Since the DMSO was applied copiously by the subject prior to the emergency room visit, it could have very well been present on their upper and lower extremities.
Those details including the exact positioning of the healthcare workers at the time of the acute poisoning event and whether DMSO was present even in the upper and lower extremities of the subject was not available to the author at the time of publishing this article. In the future, adding those details into the theoretical modeling could help predict the differential severity of exposures to DMS as well as the identification of a possible loci of defibrillator discharge related DMSO oxidation.
The resultant inhalation of those DMS vapors by the emergency room healthcare workers could accurately explain the development of sudden onset of severely debilitating, rapidly worsening symptoms among them. In addition to DMS, it was very likely that other noxious vapors were also created.
The formation of other noxious chemical vapors from DMSO acting as the precursor, can be explained using electrochemistry modeling. The chief consideration for this electrochemical decomposition model was that: the copiously dermally applied DMSO along with the high concentrations of sodium (Na+), potassium (K+) and chloride (Cl-) ions present in the sweat of the subject, which was present in unusually greater concentrations than normally would; due to the subject’s renal failure, acted as a high resistance electrolyte layer.
This electrolyte layer underwent a defibrillator mediated high-voltage electrochemical breakdown; resulting in the production of highly reactive hypochlorite and chloride anions as well as their corresponding highly reactive free radicals.
These highly reactive entities contributed to the generation of several additional noxious chemicals through the interaction between those highly reactive electrochemical breakdown by-products and DMSO.
The electrochemical modeling indicated the creation of even more highly toxic moieties during the defibrillation process, such as the formation of: methylsulfonylchloride (CH3SO2Cl), thionyl chloride (SOCl2) and sulfuryl chloride (SO2Cl2). All of these reaction products are known to be highly noxious agents upon exposure, either through the dermal route or when inhaled.
Conclusion:
The thermal decomposition model for the DMSO based on the thermal effects of a defibrillator, along with the electrochemical decomposition model for the DMSO-sweat electrolyte mixture was developed for a precise theoretical understanding of the effects of the application of high voltage electric potential across this electrochemically active layer during the defibrillation process.
The goal for creating this electrochemically active layer model was to mimic the chemical behavior of the subject’s dermal application of DMSO. This novel composite chemical reactions model helped in the addition of a new list of noxious gaseous decomposition products of DMSO as putative causative agents for this toxic exposure event in addition to the originally proposed DMS.
In summary, based on this defibrillation mediated composite thermal and electrochemical decomposition model, the most likely explanation for the acute poisoning symptoms observed among the emergency room healthcare workers who were part of the team that treated Gloria Ramirez on that fateful day; were due to either the inhalational or dermal exposure of those noxious decomposition products of DMSO as a result of application of the defibrillator.
This modeling is controversial because it raises the possibility that the subject was also potentially exposed to those DMSO decomposition products generated during the application of the defibrillator.
Since the subject already had developed an end stage renal disease, it is debatable whether such an exposure to the DMSO decomposition products contributed to the subject’s mortality, but it is very clear that such an exposure in no shape or form would have helped the subject survive that particular dysrhythmia episode. An important lesson to be learned for healthcare providers, especially those working in an emergency care setting; from this particularly difficult emergency room case, is to develop safety protocols to address the possibility of defibrillator related injuries; including those arising from defibrillation related noxious fumes.
