I’m seated here, in upholstered comfort, with two questions. The couch is a dreadful, shameless pun, which I will explain in a moment. The questions though, are real.
Both questions relate to the relevance of evolution in emergency medicine. The first is how does our current understanding of evolution help us be better clinicians? The second question is what do we not yet know? Or, in other words, what is the depth of our ignorance? (Please don’t answer that. It is a rhetorical question*).
Evolution. To briefly recap the last three and a half billion years (give or take), it started when a few basic molecules chunked themselves together. Amino acids assembled into proteins – monomers to polymers, folding themselves into proteinaceous origami. DNA formed. Pretty quickly this had the remarkable idea to split and produce an heir. This was the real miracle of life. Twitches of biological advantage then produced, amongst other things, a wall to box in the carbon-based bits and bobs forming cells – units which then really got the hang of division. They did this over and over. For a while things bided their time. These bacterial grade debutantes swum round in a vicious, blistering stew for two billion years, at the end of which they realised it was time for an upgrade. By this point they had oxygenated the planet, and some serious evolution could occur. Then any hiccoughs that might produce a biological advantage were passed on, creating more and more complex organisms. Finally humans popped up with their hardly conceivable physiology; their countless internal interactions and stupendously complex responses occurring every single second. Go on, try it, just for a moment, think about what your body is doing, simply sitting and reading. Seriously. It is too cool for words (certainly far too cool for mine).
But what does this sublimely elegant sequence of events have to do with emergency medicine? Sepsis – 3. That’s what. We were discussing the new terminology in teaching. qSOFA. (SOFA, get it? I am sorry. I really am). Sepsis has to be one of the most complex disease processes around. It is a rampaging, blazing blizzard of swirling chemicals; a genomic, metabolomic monsoon. Distressed mitochondria signaling for help, agitated endoplasmic reticulum producing misfolded proteins in panic, redundant cascades sparking up and looping back on themselves. The entire organism in disarray. All of the responses interconnected and surprisingly unique to each individual. Here at the pointy end of evolution, human pathophysiology in full-flight is an event almost too wondrous to behold. And we reduce it down to a respiratory rate, some confusion, and a 3 digit number. I fully appreciate that qSOFA is designed as a descriptor of organ dysfunction in response to infection, and is neither meant to describe, nor diagnose (I am preparing myself for the reader backlash here). But, certainly in ED, it feels so far removed from this complex and individualised disease that it hardly seems to raise an eyebrow of interest.
Rafts of guidelines we use have similar problems. How does one grind down an almost infinite array of interactive cellular combinations and permutations into a simple guideline or diagnostic algorithm? Artificial Intelligence is on its way, we are told – Holmes and Watson machines that will replace most of a doctor’s diagnostic work. Well good luck to them, I say.
To return to the original question, how does an understanding of evolution make us better clinicians? Well we can start by respecting the complexity of the response humans have to disease, and how little of it we truly understand. This way we are less likely to be prone to dogmatic statements, more respectful of the individual presentation in front of us, and more considered in our therapeutic decisions. It also helps us to understand why much of current research, on single interventions, produces small, if not no, gains (and many results seem to be simply the outcome of number-exploitation, rather than true effect).
We are the privileged few. Sometimes one can only appreciate the terrifying complexity of something when it goes wrong. We get to see it, and we are thus are not condemned to a life of sleep-walking, never appreciating the magnificence of evolution and what it means to inhabit a human body with all of its labyrinthine convoluted function.
Our second question is what is it that we don’t know? The other 99%, I would hazard a guess. Like the fact that we have just discovered 1200 new exoplanets, nine of them potentially habitable, all of these possibly with carbon, hydrogen, nitrogen, maybe even oxygen, all dancing around and thinking about getting it on. There is so much more for humans to discover. It’s an incredibly exciting time to be open-minded about new discoveries, both without and within, and be prepared to drop rigidly held teachings when we learn more. For us, it’s glycocalyces, hidden chemical messengers, brand new communication cascades, and so much more. And we are here, in medicine, taking part. We are, surely, the lucky ones. More wonder, I say. More wonder.
*A rhetorical question may not be what you think. Although the standard teaching is a question for which one already knows the answer, this is not quite true. The Greeks and Romans, who bestowed upon the world the flamboyantly wonderful figures of rhetoric, had dozens and dozens of terms and classifications for rhetorical questions (none of which they could actually agree upon. Sadly, their empires crumbled before they had a chance to tidy up the definitions). Some of the examples of rhetorical questions are: apocrisis, antiphora, epiplexis, subjectio, and epitemesis, amongst many others. Mine was an example of hypophora. I did not want you to answer it (knowing full well the extent of my own ignorance). Instead I intended to answer it, however lamely, in the remainder of the text. Those Greeks were onto something.