The Deal
BY THE TIME THE MERT helicopter bumps down on the Nightingale landing site outside the hospital in Camp Bastion, in whatever remains of the Golden Hour, the deal with death will be done. Lives will be dragged back from a point no one had previously thought possible, escaping from the place that is almost death, no looking back, one step, one pulse beat, back into the light, life. But just like in the myths that are scattered through human culture and history, where a deal to cheat death always has consequences, it would appear that the Golden Hour comes with a price.
We have known for some time that soldiers who have been injured badly enough to lose limbs don’t, in the words of my head of department, do very well. Studies of amputees from the Vietnam War show that after thirty years they experienced multiple serious long-term health consequences. Those studies have in turn generated projections of the cost of care for the British amputee cohort created in Afghanistan (£300 million or thereabouts, in case you are wondering). What all these studies have in common is that they take the amputation as the central feature of the casualty – that the problems somehow begin with the amputation itself, and the consequences of living with fewer limbs than nature intended. We are coming to understand that thinking this way may not be enough. Amputation is part of, but not entirely the cause, of the blighting of lives by severe casualty.
In 2002 a study was begun of American soldiers who had been severely injured in Iraq and Afghanistan. It went right back to the beginning of casualty, in careful measured steps. Severe injury could mean anything from musculo-skeletal damage (including, but not necessarily, amputation) to soft tissue disruption or organ damage. What all the injuries had in common was that the casualty required resuscitation in order to secure survival. The first phase of the study was concluded in 2014. It found that soldiers who had suffered and survived severe injuries were at greatly increased long-term risk of developing the significant chronic health conditions associated with old age: hypertension, diabetes, coronary artery disease and chronic kidney disease (just for starters – there are probably others). They could spot this only ten years after the earliest injuries had been sustained.
And there was more. This risk ‘followed a dose response pattern’: the more severe the injuries, the more complex the resuscitation, the greater the risk of developing these conditions earlier in life. Patients who survive severe injuries age faster than those less injured – depending on just how severe, it can be twice or even four times as fast.1 So the science seems to be telling us clearly that the extraordinary techniques of resuscitation that we saw in the back of all those helicopters in the Golden Hour were not finite, but are instead negotiations to strike a deal for the life of the casualty. And the terms of the deal are becoming clear: life now; less life, and of poorer quality, later.
This is an early interpretation of the data, but it’s thorough. The next phase, begun in 2016, looks at the possible reasons why (and quietly notes that this is all going to be so expensive).2 The authors of the research paper have a hypothesis about the mechanism of this accelerated ageing. It goes straight back to those first moments of the deadly cascade, when the body does everything it can to hang on to the life draining out of it, all the different cellular mechanisms trying to compensate for the physiological abnormality. And one in particular: inflammation.
Inflammation is how the body responds to injury – a splinter in your finger, the cold virus, bacteria, avulsive amputations, all provoke the same fundamental response. The inflammatory mechanism is a chemical reaction: a range of different chemical cell types are sent to fight the injury wherever it is. They consume dead cells and work to expand blood vessels around the insult, to get more blood carrying more oxygen and therefore more energy to living cells in the area. They weaken cell walls to make them more permeable so blood can get to the area more quickly and start the healing process, which is why the splinter scratch or a paper cut in your finger gets red, swollen and tender, and why your nose runs when you have a cold to sluice out the virus.
Inflammation isn’t self-limiting. The worse the injury, the stronger the inflammatory response. Scale up the swollen red scratch on your finger. Imagine how Mark Ormrod’s inflammatory response reacted to his loss of three limbs, not to mention the burns and other trauma from the IED that blew him up into the sky. What happens in cases like Mark’s has a name now: the inflammatory storm. Researchers looking into the genomics of inflammatory response to acute trauma reckon that up to 80 per cent of cellular pathways and functions are re-purposed in its early stages, during the Golden Hour.3 So even as life is fought for and saved, at another level the storm rages on. Or, as a vascular surgeon once explained to me so that I would absolutely understand how serious this is, the inflammatory mechanism in acute trauma means global whole-body badness.
Global whole-body badness is worst of all in injured front-line soldiers. In Britain, until November 2016, front-line soldiers were all young, fit males. In the young, inflammatory systems are raring to go, ready to match up to anything, and so that is what they do, rushing, flooding out into a system already battered from the outside, and already weakened from the inside when the soldiers are thin and hungry, as they often were in front-line positions in Afghanistan – with no fat, no reserves, nothing in the way. It’s different for girls. Female sex hormones make the inflammatory mechanisms operate more safely, protecting the female body from its hyperactivity. This may have something to do with the physical ordeal of childbirth: it depends on what kind of researcher is giving me the explanation.4
Eventually, when the bargain for life has been struck, when enough blood has been restored so that the lungs function again, and the pathophysiological shock has faded, the fluid that carried the inflammatory cells around the body begins to recede. In severe trauma it leaves behind debris in its wake, like those pictures of coastal towns and communities in Japan after the tsunami of 2011. Wreckage, toxic pollution, a body turned cannibal, full of acid, super-sensitive to further insults, especially bacterial, so very limited immune responses and much greater likelihood of sepsis (blood poisoning). Sepsis is the worst possible outcome for patients who are going to need a lot of surgery, because sepsis is a significant cause of post-operative death.
And the inflammatory storm never really goes entirely away. What may be left behind is a ‘chronic pro-inflammatory state’ – a mechanism that evolved to fix a human is itself broken, and its response is to overreact chaotically all the time. Look around at most of the complications experienced after severe injury: many of them may be due to the body being in this chronic pro-inflammatory state, working too hard and counterproductively to produce healing. So from whenever the analysis is done – three days after injury, six months into healing or a decade into living again – inflammation is likely to be at the heart of disappointing, painful, complex, expensive outcomes.
Or it might be something else, or inflammation in combination with an immune system suppressed by all that new blood being forced into it to maintain life at a more basic level. But whatever it turns out to be, this research, which looks at the specifics of severe injury and extreme resuscitation and sees them in terms of a whole life’s impact, is the most important thing in this book. It is the scientists’ answer to the hard question of what is going to happen. The work of the MERT allows us to see just how extraordinary extreme resuscitation is and how far we’ve come, but also to understand that it has consequences, this deal for life, and that it is often (but not always) only a beginning.