Over the past seven to ten years or so concern has increased among pediatric anesthesiologists about developmental delay risks in young children exposed to “anesthesia.” A corresponding concern has developed among adult specialists about post operative cognitive dysfunction and the late onset of dementia in patients who have “anesthesia” after age 60 or so.
The anesthesiology literature is just now filling with articles on these subjects but no biomarker-based studies have been conducted or published yet, to my knowledge, that can help point toward the cause or causes of these vexing and delayed neurological conditions.
Clearly “anesthesia” works by influencing synaptic functions or at least the interconnectivity of brain regions that otherwise need to be connected for consciousness and movement to be experienced. Common denominators in the background of every “anesthetic” are supplemental oxygen, reactive oxygen and nitrogen species (RONS), antioxidant ecology disruption, inflammation, and “transcriptome” activation/deactivation.
I have been stunned especially by the increase in autism rates since the mid-80s. Interestingly, increases in Alzheimer Disease and other oxidative stress-driven conditions have tracked autism, more or less. Some clinical historical perspective may be illuminating.
Administering ‘anesthesia” involves producing amnesia, analgesia, akinesis, and autonomic stability while guaranteeing oxygen delivery by using artificial atmospheres composed of air, nitrous oxide, oxygen, and volatile anesthetic drugs in combination with a variety of injectable fixed agents to allow patients to undergo noxious procedures without undue suffering.
Modern society’s reliance on these intensely unnatural combinations of gasses and drugs for an increasing array of diagnostic and invasive procedures constitutes one of civilizations most remarkable achievements, dependence upon which has accelerated over the past 50 years. It is however, probably not without (as yet) undetected cost to health, especially to children and adolescents, but also to the old and aging. More research is needed to point a way toward some answers to emerging questions about mental functional changes after anesthesia in all of these patient populations.
In the mid-1980s the first commercially viable pulse-oximeters came into use. This improved physicians’ abilities to continuously monitor arterial oxygen saturation without reliance on serial painful arterial blood gasses. Because it was now convenient to track immediate responses to even small changes in oxygen supplementation, empirical oxygen use became more popular in many medical specialties — pediatrics, anesthesiology, obstetrics, emergency and intensive care in particular.
An overlooked problem was that “O2 sat” is a proxy for arterial oxygen partial pressure, a phenomenon tightly regulated by both a finite natural atmospheric oxygen partial pressure, a delicate pro-oxidant/antioxidant balance, and the titration effects of hemoglobin’s function as the blood’s buffer against too much dissolved oxygen content being released to tissues. Under clinical hyperoxemic conditions of supplemental oxygen administration “O2 sat” readings max out at 100% while the measurable arterial oxygen partial pressure might range from 100 mmHg to almost 700 mmHg — a > 6 fold range equal to a toxic overdose.
It is no exaggeration to say that for the first time in history large numbers of patients could be routinely exposed to gasses/artificial atmospheric mixtures that evolution has equipped them to tolerate at much lower concentrations, if at all. With respect to oxygen in particular, in evolutionary terms, 500 million years of adaptation to 21% ambient oxygen could now be routinely offset on a medical whim by health care providers to achieve an “O2 sat” of 100%, a saturation that is almost always abnormal in itself from a physiological perspective.
It is also not an exaggeration to suggest injury homology exists at both the RONS and transcriptome level (eg. p53 activation) between hyperoxic and radiation exposures and that these might be additive over time.
Beginning with OB practices and extending beyond pediatric and anesthesia practices into intensive and emergency care settings it is plausible that oxidative stress induced by oxygen supplementation constitutes an overlooked historical thread in forms of cognitive neurological diseases.
Oxygen, as a supplemental drug, gets administered to mothers carrying vulnerable fetuses during labor and then to infants delivered in the delivery room. On induction and during maintenance of anesthesia hyperoxic gas mixtures are used despite the tendency of anesthetics to reduce oxygen consumption. In intensive care units patients are maintained on hyperoxic gas mixtures despite good blood gasses or in lieu of other maneuvers such as increased PEEP or ventilation mode changes that can support oxygenation. In the backs of ambulances patients are getting oxygen via masks even when data and clinical situations show it was not needed.
Unfortunately, audit studies of such practices are few and the clinical literature does not reflect what happens numerous times daily in practice. In the domain of understanding the science beneath iatrogenic oxygen use, basic science is way out in front of clinical practice. The consequences are macromolecular and their recognition is delayed if not overlooked entirely.
