Paris, 1917. A neuroscientist, Augusta Dejerine-Klumpke, arrived for work. A wind from the east carried the sound of artillery and gunfire up and down the front — a reminder that the world was at war, and was likely to be so for some time. Her work was at a hospital ward for injured soldiers, although she wasn’t there as a doctor but as an investigator, so it was really a laboratory. Everyone in the rows of beds had lost limbs in the fighting. Initially their injury was dealt with effectively, by well-practised surgeons and medical staff, and infections were managed as well as anyone knew how. The men were fitted with new limbs, made to fit their stumps properly by trained prosthetic builders. For the first few months of their new lives, everything had gone to plan. They had learned to walk again, and had returned home to their families. But none expected what came next. Their stumps swelled and reddened. Manageable pain became unbearable and their new limbs simply wouldn’t fit any more. It was as if none of the careful work of the surgeons and nurses had mattered. The patients were back in clumsy wheelchairs, crippled and useless. No-one could understand why. Doctor after doctor handled their stumps, prodded and poked them, and then stood back in puzzled silence. There was no infection, no nerve damage, no reason why their restoration should be failing so completely. Yet the evidence was there, in bed after bed.
In the final year of the war, the neuroscientist Augusta made a breakthrough. She had been taking X-rays of the failing stumps — one of the first uses of X-rays in medical research — and had noticed that what had once been neatly healing bone ends were now jagged and rough. It wasn’t the bones themselves that had grown over; it was the tissues surrounding the bone: nerves, blood vessels and especially muscles. What had once been soft tissue was becoming hard tissue — becoming bone itself. This new hard tissue affected the nerves and the stump, causing it to swell and become painful, destroying the neat profile that had been used for the prosthetic fit. Augusta noticed something else: all the soldiers had been injured in the same way. They had not been injured by gunfire or stabbed; they had all been brought down by the powerful blast of a heavy shell fired from a large artillery weapon.
From the story told on her X-rays, Augusta theorised that it was not only the metal fragments and shrapnel that had injured the men. The actual blast wave energy of the explosion had also somehow affected them, and was still affecting them long after their original injuries had healed. But then, in 1918, the Great War ended. Augusta’s ward was closed down and the men dispersed to hospitals across France. Augusta kept up her research as best she could, but without the war it lacked focus and support, so eventually she returned to her civilian research. She died in 1927, and her results, conclusions and patient-subjects faded away to live lives much impaired by the failure to resolve their condition.
Almost a century later, in another war where soldiers lost their limbs to high explosive munitions in mines and improvised explosive devices or ‘IEDs’, the medics began to notice that their amputation stumps were not healing as they should. Expensive, custom-made prosthetics stopped fitting after months or a year’s worth of normal use, and stumps became malformed due to pain and swelling. Again, scans revealed inexplicable bony growth, along nerve shafts or blood vessels or in muscle mass. It wasn’t the bones themselves, but the soft tissue around the bones turning hard. There is a name for this now: Heterotopic Ossification, or HO. It is experienced by almost 70% of military amputees whose limbs were lost as a result of blast injury. Where one scientist led a century ago, now others follow, seeking to understand the full range of physical consequences of an invisible killer: the blast of a high explosive shock wave.
While HO is experienced months or years after the original explosion, the shock wave strikes within milliseconds, surging through a human being, wreaking havoc. Blast injury is where physics meets human biology. Explosions generate very fast, very powerful increases in air pressure, transferred as a wave outwards and away from the site of the blast. The shock wave passes through the tissues, causing differences in pressure at all sites in the body where gas and liquid are contained. Bowels can rupture, with the resulting bleeding or peritonitis requiring complex treatment. Ear drums are also ruptured, and though most hearing injuries resolve themselves spontaneously, some do not, leaving the casualty with a permanent impairment, from tinnitus to deafness.
Most serious of all is the effect on the lungs. Lungs are composed almost entirely of air, bound by the thinnest of membranes which allows oxygen into the blood. The shock wave tears into this most fragile of tissues, and lays it to waste, causing swelling and haemorrhage. This injury, called ‘blast lung’, is inflicted even by moderate shock waves that do not otherwise cause significant damage, and is particularly dangerous because the damage does not stop once the wave has passed through. Instead, it gets progressively worse, asymptomatically, until it is too late. Initially if a patient presented with a burst ear drum, then blast lung was assumed. Now, all patients likely to have been exposed to a shock wave, whatever its force, are scanned for blast lung and treated for blood loss, and with oxygen therapy to restore lung tissue.
Organ by organ, researchers are consolidating our understanding of what happens as the blast wave travels through our bodies. The immediate effects are understood, but conditions such as Heterotopic Ossification (HO) give clear indications that long-term effects are also initiated at the moment of wave impact. These are complicated and difficult to treat, and researching them requires a multidisciplinary team of scientists and clinicians. A consensus is appearing: shock waves may trigger or distort the body’s own inflammatory response, altering it at the genetic level. This appears to be the explanation for what happens in the formation of HO. One possible way to mitigate the effects of blast injury is an early intervention at the genetic level to restore or normalise the inflammatory response mechanism.
However, perhaps the most serious threat to blast injury casualties is our inability to consolidate research gains made during wartime. Medical history shows that we are always efficient at treating the immediate emergencies of wounds, but have not been able to sustain work to resolve the broader issues, like pain in its various forms, and head injury — that we now call Traumatic Brain Injury. Imagine if the 1917 research had been formalised into a research programme that had run consistently for a century. It isn’t hard to imagine that our understanding of cellular biology, of pain and of bioengineering would have been considerably further advanced than it is now. Just because we no longer hear the sound of artillery or mines exploding, doesn’t mean we should forget what happens when they do.