I should have known . . .

It’s fairly evident that I really REALLY need to clarify what I meant, and what I didn’t mean, by my comments concerning “errors in judgment”. I see that I’m being quoted a lot, in lots of outlets. That’s not a problem of course, but it becomes problematic when what i wrote is turned into something that I most certainly did not say.

1) I am strictly referring to the period of management BEFORE Michael was admitted to Grenoble. As I said on 30 December, the people taking care of Michael in Grenoble can take care of any member of my family any day. They are professional and more than competent. This is an impressive team and they deserve to be recognised as such.

2) I am in no way criticising ANY member of the care team(s) dispatched to fetch Michael on the slope, nor of those involved in transferring him from Moutiers to Grenoble. As I made clear, prehospital medicine is difficult under the best of conditions. It’s not hard to imagine the added stress faced by the guys on the slopes, confronted with a clearly injured mega-star, and what must have been a VERY difficult entourage to manage. I don’t have sufficient facts of any kind, and it’s neither my job, my business, nor my intention to question the individual medical care provided by my colleagues.

What then exactly AM I saying, and almost as importantly, WHY am i saying it here, and why now? These are valid questions, and they deserve an answer.

3) I am very clearly criticising a system that allows head injured patients to be brought to non-neurosurgical centers, in the absence of other clear reasons to do so.

4) The failure to adequately control an agitated patient prior to flight, as well as the delays in adequate control of the airway likely indicate insufficient training, insufficiently robust protocols, and perhaps insufficient experience under difficult circumstances (again, a mega-star patient with a difficult, demanding and perhaps even frankly hostile entourage). I am very clearly criticising a system that allows this to happen.

5) It is impossible to quantify the impact of the above on outcome in Michael’s case. Obviously. It is also obvious that someone whose neurosurgeon, the day after the trauma, describes his condition as “hematomas left, right and centre” is likely not to do particularly well. This should be obvious, at least to the “journalists” who disingenuously (at best!) implied that I said that Michael’s current situation is because of these aspects of his initial care. The delay in admission to a neurosurgeon, as well as deferred airway control, cannot have been good for a severely injured brain. Especially in a situation where the intracranial pressure has risen so high that parts of the brain are literally being squeezed out of the cranial vault. That said, in terms of prognosis, this likely pales in significance compared to the 2000-and-some-odd joules of impact energy against that goddamned rock.

The world of medicine, including the practice of prehospital medicine, has become more and more evidence- and protocol-based. This requires constant attention to new developments, and elaboration of consensuses that are often universal (for example, the algorithms of basic and advanced life support). Intense and rigorous adherence to these protocols, with the training that this implies, has been shown to very favourably impact on the outcome after trauma. I will simply say that the French have been remarkably, and unexplainably, recalcitrant to this notion of protocol-based medicine.

Why have I said this now?

I want to make it clear that the furthest thing from my mind was causing Michael’s family added pain. Malpractice? Hey, I work in Europe, which is far from having gone as nuts as the USA with this. In any event, I don’t give a shit about MAL practice. What I’m concerned with is GOOD practice. I want people who’ve not thought about it previously to now think, before heading down the hill on their skis or boards, “am I going to be well looked after, by people with sufficient knowledge, skills and maturity, if I have an accident”? And I want the answer to be yes. Wherever, whenever.

Those of you who know me a little know that if I’ve contributed anything to motorsport medicine, it’s been mainly down to education and training. The book, the systematic simulation exercises at every Grand Prix, etc. Doctors are nothing if not people who never stop, and never want to stop, learning. I think we need once again to make sure that people who do prehospital medicine, who routinely face life-threatening situations, are sufficiently trained, equipped, and mature, to carry out their duties impeccably.

With that in mind, I need to send a quick and heartfelt shout out to General Zin and the medical team at the Grand Prix of Malaysia. These guys have created a society for motorsport and traffic medicine, with a goal to fostering best practice in the community of caregivers doing this type of medicine. BRAVO!!! These guys are tops, and have been for some time. To illustrate how “on it” they are, they have the only circuit medical centre to be ISO certified. And they’re my friends!

It’s just a pity that the national federations are left alone to carry out initiatives like this (needn’t remind you of my attempts at organising an international society!), without leadership from Paris. Again Mr. Todt, it’s not because you gave your mates fancy titles that they have, by magic, acquired competency in this field. Motorsport medicine is stagnating, and will continue to do so as long as there is a total lack of leadership from the top.

Odds and ends

Well it’s been a long time, hasn’t it? As always, I follow your comments closely, both here and on Twitter, and I think it’s time to address some of the points that have been raised recently, and perhaps clarify a few definitions (nothing new here, pretty sure this stuff was covered in earlier posts) – simply because I’ve got a feeling that we’ll be hearing some of them at some point in the not-distant future. More on this later.

WEIGHT LOSS

I’ve been asked about the report that Michael has lost 25% of his pre-accident weight.

This is entirely possible, and in fact, probable. A few factors explain this. First, the initial injury, operations, and those few harrowing weeks when Michael’s life itself hung in the balance, minute-to-minute. This kind of situation subjects the body to a tremendous level of stress. Not psychological stress, mind you, but physical stress, accompanied by liberation of massive quantities of stress hormones. These hormones evolved for the “fight or flight” response, and were designed by evolution to promptly mobilise fuel for action. They do this by causing (among other things) breakdown of muscle to form amino acids, which the body can use as fuel. The problem is that when these stress hormones remain present for too long, it becomes very difficult if not impossible to replace the lost muscle mass, at least in the short term.

So Michael’s muscle mass was already fairly significantly depleted by the time sedation was stopped. At this point, what is usually called disuse atrophy starts eating away at the muscles. Since a patient in coma has very little, if any, movement, the muscles lose the mechanical stimulus that is a major factor in maintaining them during normal day-to-day activity. And although coma patients get intensive physical therapy, this is aimed at preventing the joints from stiffening, not at maintaining (or building) muscle mass.

There may well be a more subtle contributing factor as well. You see, the normal brain kicks out growth hormone at night, during our sleep. This hormone helps the body to build and maintain itself, notably by helping the muscles take up protein. It is entirely possible, even probable, that this pulsed pattern of secretion is lost (any neurosurgeons reading this, or neurologists, anyone in the know, just jump in!) in patients who no longer have sleep-wake cycles. It’s even possible that secretion of the hormone falls to very low levels chronically. This would also have the effect of taking away an important “trophic” stimulus.

Happily, the consequences are not particularly dramatic, at least immediately. To be blunt, a patient in coma doesn’t really NEED his or her muscles . . . with the exception of the diaphragm. The diaphragm, which like the heart is pretty much always active, resists atrophy rather better than other muscles, but it does atrophy. And having a machine doing the breathing for you is one of the best ways to see how disuse atrophy affects the diaphragm too. Unfortunately, and assuming (as I have until now) that Michael is being ventilated by a respirator, there is probably some degree of diaphragmatic atrophy at this point.

Now remember where Michael is coming from – one of the fittest, toned, and conditioned 45 year-old men on the planet. This means that if and when he can be weaned from mechanical ventilation, re-training his diaphragm shouldn’t be problematic. As for the rest of his muscle mass, should he awaken, the same ferocious appetite for pushing himself will no doubt lead him back to most of his former superb condition.

TRANSFER

I’ve also been asked why Michael hasn’t been transferred to a unit closer to his home.

Obviously I have no idea of the answer to this question, but several factors need to be considered.

First, from a medical point of view, once we’re out of the phase with dramatic and life-threatening elevated intracranial pressure, and barring other significant problems causing physiologic instability, the patient can be transferred arbitrarily far. The transfer needs to be prepared carefully, of course, but even hours-long flights are possible with intubated, ventilated patients such as Michael. So why is he still in Grenoble? I’m basing myself on the notion that Michael is still in the Intensive Care Unit, and is still being ventilated.

First of all, it clearly shows that his entourage is totally confident with the quality of care Michael is receiving.

It’s important to remember that Intensive Care Unit (ICU) beds are a very limited resource. Every day intensivists are asked to admit critically ill patients to units whose beds are all filled. This requires TRIAGE – deciding who has the best chance of being improved by being admitted to the unit. The “chronically critically ill”, patients like Michael who depend on technology (a ventilator) to stay alive, are a tremendous conundrum for ICU personnel. As time goes on (more detail below), it becomes less and less likely that Michael will emerge to any significant extent. Therefore, I think it is inevitable that should the status quo continue, the ICU staff may well, at some point in the not-distant future, decide that the patient they’ve just been asked to admit has a higher need for that bed than Michael, given his clinical situation and prognosis. This then could be a reason to organise a transfer – to a private clinic, or to an ICU-like environment that his entourage could build at his home.

Lastly, as I’ve mentioned furtively here and there, I think that serious lapses in judgement were evident during Michael’s initial management (I have this from usually impeccable sources who have access to this information). Because these lapses could (and almost certainly did) worsen the outcome in Michael’s case, it is possible that the staff at Grenoble feel duty-bound to NOT place any pressure on the family to transfer out, despite the terribly dismal prognosis . . . because of the clear (but unquantifiable) contribution of medical misjudgement to that prognosis.

(RE) DEFINITIONS

I think it’s useful to look at a few definitions again, briefly, for when this all starts to get talked about in the press, as I’m sure it will be fairly soon.

Brain Death: A brain-dead patient is dead. There is objective, demonstrable, and irreversible cessation of ALL brain function. When you use arteriography (special x-rays that show the arteries and the flow in them) to look at the blood flow to the brain, you see that there is NO BLOOD FLOW AT ALL inside the cranial vault. There is no reaction to any stimuli except for simple reflexes (which originate at the spinal level), and the patient will not breathe spontaneously, even when carbon dioxide levels are elevated. There are no living brain cells in the skull. None. At all. Families do not have to approve disconnecting these patients, as they actually are no longer patients, they are . . . dead. These are the patients who become, under certain well-defined circumstances, organ donors. Because the brain, all of it, is needed for the body to survive satisfactorily, the hearts of brain dead patients will not continue to beat more than a few days or weeks (a few cases of longer circulatory persistence have been described but this is vanishingly rare), despite the most aggressive treatment possible.

Coma: coma is defined as a state where the patient shows neither wakefulness nor awareness. So the patient in a coma has closed eyes, shows no evidence of a “sleep/wake” cycle, and shows absolutely no sign of any awareness of (or interaction with) either the environment or him/herself. Even painful stimuli fail to cause meaningful interaction. Depending on the areas that are damaged, these patients may or may not breathe on their own. That said, they will essentially always be intubated, and then tracheotomised, to prevent episodes of airway obstruction caused by the brain being unable to coordinate the muscles of the tongue, pharynx and voice box. They are initially fed by a tube passed through the nose to the stomach, and later (as is no doubt the case with Michael) by a tube placed directly into the stomach or small intestine through the abdominal wall. Usually a coma is defined as persistent when it has lasted more than two months after the precipitating event. For info, I assume this is Michael’s current status.

Whereas brain death is inevitably followed by circulatory death within days to weeks, patients in a persistent coma have somewhat brain function, especially in areas associated with maintenance of physiological stability (body temperature, blood pressure, water volume, etc). This means that the life expectancy for a comatose patient who does not improve neurologically is measured in months to a relatively few years. Once again, the brain is necessary to integrate those of the body’s activities which contribute to a normal lifespan.

Persistent vegetative state: here we must distinguish two things that almost always go together: wakefulness and awareness. Patients in a persistent vegetative state show signs of “wakefulness”, in that they have periods of spontaneous eye opening, and can even show cycles that resemble sleep-wake cycles. They are, however, unaware. There is a total, rigorous lack of any sign of self awareness (including pain, other than reflex responses, thirst, etc) or of the environment. These patients often breathe for themselves.

A vegetative state is defined as persistent when it lasts two months after the precipitating event. As we’ve mentioned previously, the longer one remains in a vegetative state, the less the likelihood of emerging, and the higher the chances of severe sequelae if the patient does in fact emerge. Most definitions consider the vegetative state to be permanent one year after the injury.

Patients who are in a persistent/permanent vegetative state have lifespans that are measured in months to a few years. This depends on baseline function (extraordinary in the case of Michael, of course), the quality of nursing care, and other imponderables. They usually die of respiratory or urinary infections. Longer survivals have been described, but are exceptional.

Minimally conscious state: here, as with the vegetative state, there is wakefulness. But here, there are signs, inconsistent, variable, but clear, objective, and reproducible signs of awareness: interaction with the environment and/or of self. Like what? Eye tracking, motor responses, smiling, turning the head consistently to voices, etc. Or appropriate reactions to stimuli. This state can also be persistent; it is significant because it represents the first stage out of the vegetative state on the continuum towards normal consciousness . . . and the first interactions the entourage sees from their loved one.

Minimally conscious patients also have a severely shortened life expectancy, but not quite as dismal as for “deeper” levels of disordered consciousness.

PERSONAL NOTE

I always knew Michael was adored. I spent years at circuits drenched in red by the ferrari caps, flags, and shirts, and all of that for Michael. I’m still staggered by the depth and persistence of his fans’ love for him. And whereas I worried more than a bit about what was going to happen when and if really bad news got announced, I’ve realised that perhaps the lack of status updates has given us all a chance to move on a bit, to process what’s happening, and to start to . . . detach. And I think this is probably one of the unexpected “benefits” to the media strategy chosen by Michael’s family. Somehow, I get the feeling that people are going to be ok, no matter what happens, because they’ve now had the time to process this all. I just regret that to get here, you’ve all had to work through feeling abandoned. That will go away too. I hope.

Only a miracle

So now the Telegraph is reporting that the doctors caring for Michael have told his family that “only a miracle can save him”.

1) doctors, no matter their spiritual bent, do NOT talk to patient’s families about miracles saving anyone. Ever. From a practical viewpoint, this gives a patient’s family absolutely NO useful information on which to act. It provides hope, yes, but not for anything with any medical reality. And this hope will then cloud all subsequent decision-making.

A statement like this is more than ambiguous – it lets each recipient interpret it in his or her own context, the opposite of clear precise information. What would the care team mean with a statement like this? Are they saying “let’s wait a bit more for the miracle”? Or are they saying “miracles don’t happen in reality so we’re pretty much out of hope”?

I can only guess that what this report means by “save” is “recover sufficiently to have meaningful interactions with his loved ones”. So you see why this is kinda a dumb thing to say. And why it is impossible for me to imagine doctors EVER communicating like this with a grievously injured patient’s family.

If something like this WAS said, I can only try to “reverse engineer” it, and from there consider what they were saying and how it’d be said.

1) If there is now clinical, radiologic, physiologic and other data that leads to the conclusion that a resumption of any meaningful consciousness at all is impossible (see? no mention of miracles), they would be VERY unambiguous with this. In a situation like this, there must be no guesswork – NONE on the part of the medical team, who need to put the data together and reach an unquestioned and unquestionable conclusion. In this situation, ANY ambiguity in communication with the family is disastrous. They will often cling to any hope left, and this conversation is going to be, tragically, THE conversation that finally (and gently and compassionately) needs to remove all hope. This is crucial. If the message is misunderstood, it will almost inevitably lead to major problems, conflicts and tension subsequently.

Let me just say here that medical ethics allow, and virtually require, doctors to refuse to provide treatments they reasonably consider to be futile. My neighbour cannot show up at the hospital and demand that a surgeon remove her appendix. And in the above situation, where there is incontrovertible evidence of damage so severe as to make resumption of consciousness impossible,  doctors can certainly undertake the process of “therapeutic de-escalation”. Even if the patient’s family insists that “everything be done”, if there is NOTHING left to be done, there is no requirement to do anything more. At that point the patient’s family can make other care arrangements. It’s obviously critical to avoid this kind of situation, so once again you see the need for perfectly clear, concise information, with no ambiguity. Families need time to accept this, whether it’s in intensive care, or oncology, or genetic anomalies, and so on. But with open honest and clear communication, this will happen.

Please note that this is NOT the situation for a patient in a persistent vegetative state, at least not necessarily. This is the situation for a patient whose condition is even WORSE. The essential point is that the impossibility of recovery has to be as certain as current medical science can be AND that this certainty be transmitted to the family.

2) if the clinical situation is desperate, but not without all hope, the family would be told this, with as close to numerical precision as possible. In a situation where there is hope, it mustn’t EVER be taken away. On the other hand, families need to know, at the most basic level, that most patients like this get better, or that a few get better, or that really VERY few do. That 60%, or 20%, or 1% get better. No talk of miracles.

As I mentioned a few posts ago, if this conversation has happened, if Michael’s family has been told that it is extremely unlikely that he recover “satisfactorily”, then it is quite possible that the “several steps of separation effect” between hospital personnel and the press could have led to this kind of language appearing in these articles.

And again, despite a day during which we’ve been told Michael is breathing on his own AND that it would take a miracle to save him, we know nothing more than we knew yesterday or the day before.

This helmet cam stuff

Those of you who follow me on Twitter might have seen, in between the (well-deserved) rants about Putin, a long series of tweets about helmet issues. These were in answer to @jameyprice, who I’d like to thank for “inspiring” this. It’s something I meant to get to anyway, and I think the time is right.

But before we get to that (oh I should be in advertising) I also wanted to say that I read every comment any of you post. In detail. There are tons that I’d love to answer, and that deserve an answer for any of a number of reasons. I just don’t have the time! I’ll probably make notes and then blog answers in one fell swoop.

Don’t even think about asking about fell swoops. I have no idea what they are.

So. The question is whether having a helmet cam made the impact more severe.

I believe it was concluded that the camera had no influence on the severity of the injury. I will admit to not having read the report. But I’ll tell you what I know about this aspect of helmets. It also helps to understand a bit more about the mechanisms of head injury.

If we confine our analysis to linear forces, I think it’s reasonable to conclude (if the attachment was via suction cups, double-stick tape, etc i.e. a NON-invasive attachment) that the camera probably didn’t significantly weaken the helmet. The camera no doubt broke away on initial impact.

That said, I think it’s important to understand some of the more subtle problems with helmet appendages . . . of any kind.

Almost any interaction with its environment will make a helmet, and the head it contains, turn. Now this may only be a very few degrees, but the point is that the turning movement is an acceleration. Imagine an open wheel car having an angled frontal impact. The driver’s head pitches forward and to the side. As it contacts the cockpit side rest, an ANGULAR ACCELERATION , measured in (I think) radians per second per second, is produced. Since the head turns in a very short timespan, it all means very high acceleration. It’s intuitively obvious that any part of a helmet which increases interaction with the environment also increases angular acceleration (frictionally as in the example above, mechanically as with a helmet cam hitting a rock, or aerodynamically with the various aero appendages on modern racing headgear).

Why is this important?

Let’s take two nested tupperware bowls, put some foam between them. Oh yeah – the inside bowl contains jello, covered with some cling film. Let’s turn them over, and jam it all onto a piece of broomstick. Outer bowl =  helmet, inner bowl = skull. Jello = brain, and, yep, the broomstick is the brainstem.

Now we’ll grab the outer bowl, and twist it about 10° REALLY fast.

The “helmet’s” motion is coupled to the “skull”. The coupling is neither instantaneous nor perfect. The weight of the helmet’s contents cause some delays, as would any degree of slippage of the helmet. No matter.

Once the skull bowl has begun turning, the jello does too, but with another lag, And then, the jello brain transmits rotational energy to the broomstick brainstem. And again, there’s a lag. If you imagine some orange slices INSIDE the jello (thanks mom!) you can even imagine this kind of differential rotation occurring within the brain itself.

Each time contiguous structures are rotating at different speeds a SHEAR force is created. Shear forces are exactly what they sound like – forces acting parallel to each other but in opposite directions.

What’s shear doing at the skull-brain interface? Well among other things, it causes hematomas by tearing delicate veins running right there between the skull and the brain. That’s bad of course, for all the reasons we’ve spoken about in previous posts. Unfortunately, this can also happen WITHIN the brain itself, at areas of differing structural properties. And again, tearing of nerve tracts and blood vessels can occur in these areas. Damage and intracerebral hematomas result.

Worse still is what happens at the interface of the brain with the brainstem. Remember that the brainstem, in addition to maintaining and regulating the vital functions (breathing, blood pressure, etc), also sets up awakening and arousal of the brain. When rotational acceleration causes damage here, it is often devastating. Basically, these patients don’t wake up.

Because of how dramatically they contribute to the severity of head injury, helmet interactions with the environment, and the rotational acceleration they induce, need to be considered when designing a helmet for a specific purpose.

I cannot possibly know to what extent any of this contributed to Michael’s injuries. I, like most of you, am very preoccupied by the silence from Grenoble.

You guys are pretty amazing

Wow – if I was amazed before at your comments, I’m totally staggered by all the feedback from the previous post. I’m staggered by the depth of your thought and reflection, by your eloquence, and by your willingness to sit down and join the conversation.

You’ve made me realise I was certainly too strong in my criticism of the current comms policy. You’ve probably noticed this is a bit of a character trait! I’m exquisitely sensitive to the unimaginable situation Michael’s family and friends are in, and if I could think of how giving us SOME information would make their lives in any way worse, I would reverse position immediately.

I do feel strongly that there’s an implicit contract, whose terms are negotiated in real time, between celebrities and their public. Paparazzi can take and publish pictures of celebrities during “private” moments that they can’t take of any of us. That’s been established as a legal principle. The line they and others either respect or step over is also defined in real time, by judges, juries, and by societal mores. But it seems a bit one-sided to want the benefits of celebrity yet retain all the perquisites of a full private citizen outside of, say, the circuit. Once again, I don’t mean this to say that all discretion, all privacy, are sacrificed to the altar of the public’s obsession to “know”, but simply that there’s a line, a very squiggly changing line, that needs to be plotted.

Once again, thanks so much for taking the time to write. I’ve learned so much, and been forced to think so much, from your input. That’s exciting and sobering, and is an immense privilege.

Frank – you’re gone coz no matter how strongly you feel about anything, this isn’t the place for vitriol. Tone it down, and read these comments before writing – smart, well thought out, passionate. You can call ME whatever you want; I’ve heard it before and will certainly hear it again. But don’t even THINK about insulting my readers.

Perplexity

I’ll admit to being perplexed.

First, about the silence from Grenoble.

If you’re not in the habit of reading the comments section after each post (I do, of course – it’s wonderful to see what those of you who read me think, and a source of wonder that you’d actually take the time to write), it’s worth a look (in chronological order) at the comments to my last entry.

It’s pretty clear that Michael’s fans are beginning to feel like their devotion, commitment, and passion for someone they’ve elevated to hero status over many years means nothing. I see strains of anger, disappointment, frustration. Others, with considerable self-abnegation, are hewing to “respect for Michael’s privacy” and accepting the lack of information with equanimity . . . but even here there is an undertone of frustration at being asked to do so.

I’m not a journalist, and I’m not a PR/communications professional. But I totally fail to see how the current comms policy helps either Michael or his family. I fail to see how talking to us about the significant ups and downs of this long hard process damages Michael’s privacy or makes Corinna and the kids’ journey more difficult. I cannot possibly understand the reasons for any of this. I’ve said it before, and I’ll repeat it. This is totally unfair to the people who made Michael the celebrity he is. The people who vibrated to his victories, and were saddened by his defeats. They deserve to be told something. I didn’t say it’s their right to know (although jurisprudence places looser limits on celebrities’ “privacy” than on that of “normal” citizens); rather I said they DESERVE to know. Why on earth is their pain not being considered? How is keeping the millions of fans in the dark helping ANYTHING?

I’m also a bit perplexed about this latest thing in FOCUS.DE about re-starting the sedation. First of all, the article is rather remarkably poorly written. That, plus a singular lack of content make it useless, and surely not even worth wasting one’s time reading.

With no knowledge of Michael’s current clinical condition, it’s impossible to say why he would be re-sedated at this stage. Generically, any situation requiring a still, tranquil patient might raise consideration of reinstating sedation. This could be, for example, respiratory deterioration that requires a new period of mechanical ventilation. It could mean that there has been a change in his neurological status, with perhaps some signs of agitation, or a systemic infection originating in one of the several catheters still present. Again, we have absolutely no idea.

Right now I’ve really only one question (that predates the re-sedation issue). Has Michael been weaned from the ventilator?

As I’ve mentioned, once the sedation was stopped, the next big step physiologically speaking was respiratory weaning. This appears to me to be a piece of news that is unequivocally good, and therefore I cannot imagine it being held from the public. Imagine having heard Sabine say “I’m happy to say Michael is now breathing on his own”. Once again, if he HAS been weaned and we’ve not been told, then this is a shameful and arrogant neglect of his fan base and the public.

If on the other hand Michael is still dependent on the ventilator, it’s important to look at why. In this case, that of a young and (remarkably) healthy man with a high probability of brainstem lesions, damage to the respiratory centres would be high on the list of reasons.

Damage to the brainstem can be associated with numerous clinical presentations. It is where breathing is controlled. As important, the brainstem contains structures that play a vital role in waking the brain and maintaining wakefulness and attention. It’s also where the nerves to and from the face (for hearing, sight, taste, feeling and movement) enter the brain.

With sufficiently widespread damage to the brainstem, the patient shows no sign of awakening, and remains ventilator dependent. This is obviously a devastating situation. Brainstem injury is suspected based on the clinical status of the patient, and is then sought using imaging, especially MRI scanning. The actual function of the brainstem can be interrogated using several techniques, including what are called “brainstem auditory evoked potentials”. This involves placing headphones on the patient and playing a series of several thousand clicks through them. Then, sophisticated software is used to detect, embedded within the electroencephalogram, the passage of the sound information through the brainstem (where it enters and undergoes initial processing).

Let’s cut to the chase.

If Michael is not breathing on his own, and is (as we suspect) not showing signs of purposeful interaction with his environment (I am ignoring the mouth movements of which Felipe Massa spoke), AND if there is imaging and functional evidence of extensive and irreversible brainstem damage, Michael’s doctors will discuss withdrawing treatment with the family, as under these circumstances there is essentially no chance of recovery. It is possible that this discussion has already happened.

If Michael is breathing on his own but still not showing purposeful interaction with his environment, then patience is still very much in order. Remember that at one month post-sedation, persistence of this state means roughly a 50% chance of awakening, with the quality of that awakening an open question. This falls to 20% at six weeks (three weeks from now), with a larger portion of these patients having severe functional handicaps. And at one year, essentially no one still comatose wakes up.

Lastly, if Michael is breathing on his own AND showing signs of meaningful interaction with his environment (I very much hope, but very much doubt that this is the situation), then a certain number of people should be ashamed of themselves for denying this good news to his fans. If there is indeed progress and good news ready to be told, then the current comms strategy will go down in the annals as among the most ill-guided, unprofessional, and hurtful in the history of Formula 1 PR.

What should we be thinking now?

It’s just about two weeks since the team caring for Michael Schumacher stopped administering sedatives in order to allow him to emerge from the pharmacologic part of his depressed consciousness. Where are we now?

As usual, a few caveats. I am not receiving medical information from Grenoble. I am basing most of what I say on experience-related conjecture, as well as cautious interpretation of whatever is leaking from the hospital. This obviously means that it all needs to be taken with a rather large grain of salt!

I’m assuming, taking as axiomatic, that if there was significant good news we would be told. Despite the totally understandable need of Michael’s family for privacy and “space”, Michael is a public figure, admired and revered throughout the world. It’s the public who largely made Michael the hero he is to so many. If my assumption is wrong, if there has been a decision to effectively embargo all news, then I think this is somewhat unjust, unfair, and maybe even a strategic error in terms of communications. What’s more, it automatically means the only “information” we get is from leaks.

I’ve heard that the hospital staff is warned every day about protecting confidentiality. This is normal – but so is a passing comment made by a staff member to a friend or family member (prefaced of course by “you mustn’t tell anyone” and relayed in turn to another, trusted person, but still preceded by “you mustn’t tell anyone”) that then gets relayed to a journalist, hungry for anything to write. This is usually a tabloid, as only they would publish such unconfirmed stuff. So in the current state of affairs, I’m somewhat inclined to accord Bild’s latest output “there’s rarely smoke without fire” status. For what it’s worth.

First, as to the “gradual” reduction in the sedation.

In terms of the pharmacology of ICU sedation, we tend to use drugs that are eliminated quickly. This is to allow rapid adjustments in the level of sedation. Several drugs fit the bill; the actual choice depends on local practice, patient characteristics, and the objective of the sedation. 

I’ve seen one article that implies that Michael was sedated using anaesthetic gases. It correctly points out that after prolonged administration these agents take considerable time to be eliminated. It is almost certain that these were NOT used. While some ICUs (as opposed of course to operating rooms) use anaesthetic gases, it is rare, requires special equipment, and has numerous drawbacks. And IF anaesthetic gases were turned off two weeks ago, well there’s none left ANYWHERE in Michael’s body, for over a week now. So much for “coaxing the last molecules” from his body, as I saw written somewhere!

As I’ve mentioned, it’s quite possible (in fact highly likely) that a long-acting agent (a barbiturate) was used as a sedative during the period with what appears to have been dangerously high and resistant intracranial pressure. These agents would almost certainly NOT have been administered for more than 5-10 days at the beginning of Michael’s care. They would simply have been stopped, not weaned, and another agent (or agents) with much shorter actions would be started. In a young fit patient with normal liver and kidney function (certainly the case with Michael), the barbiturates would have been cleared within three to five days – but remember, shorter acting agents were started when the barbiturate phase stopped. These agents have such a fast on/off that they have to be administered continuously (by carefully calibrated pumps). This phase of sedation would be based around either propofol or a cousin of valium (a benzodiazpine), usually with a low-dose infusion of a morphine relative.

When the time has come to stop the sedation, it is usually just . . . stopped. I mentioned this in my previous blog post. Any problems along the way are usually cause to re-start the sedation, and make another attempt at stopping later. It is very rare that the first attempt succeeds. That said, it is two weeks since we were told that the sedation was being stopped. I think it’s a very fair assumption at this point that sedation has been stopped sufficiently long for there to be no residual pharmacologic effects.

Still with me? I never fail to amaze myself with just how wordy i am . . .

If my assumption is correct as to sedation, the next question I’d ask would be about ventilatory support. I hope Michael is breathing unassisted at this point, through the tracheostomy that has no doubt been placed two or so weeks ago. This qualifies as some of the good news I spoke about above. If Michael is indeed autonomous from a respiratory point of view, it’s a milestone. And one about which I think you deserve to be told. Again, I assume that this has been accomplished. If on the other hand Michael cannot be weaned from the respirator, especially if this is because of lack of ventilatory drive, this is more than ominous. At this phase post injury and post sedation, this kind of strong evidence of severe brainstem dysfunction (especially if corroborated by other testing) would likely prompt discussion with the family about withdrawing support. I do not think that this is the situation. At least I truly hope not.

If ventilatory weaning has been successful, the next question one asks is what is Michael’s level of reactivity with the environment. It’s here that we need to think about the Bild report. 

The motor response of a head injured patient is one of the most important prognostic indicators. People involved in caring for head injured patients use a standardised scoring system (called the Glasgow Coma Score, or GCS) in order to do this. The motor component of the GCS has six steps. These range from obeying simple commands (stick out your tongue, put your thumb up, etc) down to no reaction at all. In between, on the way “down” from obeying, one sees progressively less organisation in the response. Makes sense.

So IF what Bild says is true (and I looked on their site summarily, but didn’t see where this was said), we need to figure out what they meant by “no reaction to external stimulus”. If there is no response at all to painful stimulation, not even archaic stereotypical responses organised deep within ancient parts of the brain, then this is very bad news indeed. This would likely imply extensive damage to the brainstem, and at this stage post injury would, I think, be associated with a patient who was also dependent on the ventilator, as mentioned above. I would simply note, as one of those things I wish I had never heard, that when the neurosurgeon spoke about hematomas “left, right and centre”, this is what I feared. The brainstem is one of those things in the centre… 

If the motor response to external stimulation is one of the primitive stereotypical responses, this is bad news but leaves hope of some level of recovery. Numbers? Well, this level of response would indicate the persistence of a vegetative state, but roughly 50% of these patients emerge, usually with some level of residual dysfunction.

To be honest, based on Bild I don’t think any other reactions (all of which are MORE organised than what I mentioned) would lead someone familiar with the care of these patients to say he’s not reacting.

Upshot: not good. Starting to be really not good.

Lastly, I spent three days last week teaching on a trauma course with a bunch of motorsport medicine mates. One of them is a professional neurointensivist. He works in one of England’s regional neurointensive care centres. They get 600 PATIENTS LIKE MICHAEL A YEAR. One regional centre. That means that we’re all just 2 or so degrees of separation from someone affected by this. So I really hope that more than just provide “information” about Michael’s condition, I hope my “head injury” blog entries sensitise us to this devastating society-wide plague.

Stopping the sedation!

Let’s be unambiguous about this – the announcement that Michael’s care team is discontinuing his sedation is the news we’ve been waiting for. It’s the first big transition – from acute, life-threatening head injury to subacute recovery. Followed no doubt, let’s not forget, by a chronic rehabilitation phase. But this is wonderful news.

In terms of how this is done, well it’s actually pretty simple. The electronic pumps driving the continuous infusions of the sedative drugs are turned off. That’s it. But doing that means that the people taking care of Michael have a reasonable expectation that he will not exhibit untoward reactions to the “stress” of these medicines being turned off. The most undesirable of these would be elevations in . . . you guessed it . . . intracranial pressure, but to be honest, we’re now more than four weeks post-injury, and I’d rather think that we’re past that.

So what will happen now that this stuff is turned off?

1) It may or may not be true that, in general, French neurointensivists maintain sedation longer than their Anglo-Saxon colleagues. It doesn’t matter. The people taking care of Michael know what they’re doing.

2) while it’s possible that a long-acting drug may well have been used in the early, “suppressive” phase of Michael’s care, it’s quite likely that if so, it’s been replaced with one or more short-acting substances. These usually allow signs of emergence to appear within several hours of stopping the infusions.

3) What actually happens? Well in general, the first attempt to stop sedation usually gets interrupted by something. The patient gets agitated, the blood pressure goes up, the oxygen saturation goes down . . . something. So you turn the sedation back on, let the situation settle down, and then either try again or wait until tomorrow. It often takes a few tries before everything goes the way it should.

How should it go? Well ideally Michael will start to want to breathe, and allow weaning from ventilatory support. And just as important of course he will hopefully start to show meaningful interaction with his environment. Following simple commands, visual tracking, etc.

Now I’ve heard (from unconfirmed sources), unconfirmed reports (double “unconfirmed” should ring alarm bells of course) that Michael has indeed already done this.

I’d love any neurosurgeons to jump in and comment, but if this indeed is true, it is fairly astonishingly good (but indeed totally conceivable) news. So we need to cross our fingers and hope something like this DOES get confirmed in the future.

Tell you what – let’s not talk about any other alternatives right now, ok, so we keep it positive.

One last thing.

I’ve seen some very heartfelt comments here and there about articles, tv pieces, and blog speculation “hurting” Michael’s family. I wanted to just weigh in for a second.

I’ve been pretty harsh with the tabloid press, and deservedly so. But not because the Daily Mail’s moronity hurts Corinna, Gina Maria and Mick. ARE YOU KIDDING? Could they possibly hurt more? And if so, is it likely to be because of the suffering induced by a British rag? Of course not. I think it’s detestable coz it’s shit “journalism”. I kinda don’t think it’s on Corinna’s reading list, I don’t think their “journalism” could possibly add to their pain, and lastly, Michael’s care team have no doubt been TOTALLY up front with the family. Meaning they have a better idea than any of us of just what the . . . hell . . . is up.

If I thought for a second that anything I’ve written might hurt Michael or his family, I’d not have written it. To be honest, I’ve spoken to you as I’d speak to Michael’s family. I assume you know that, because I think it’s to THAT that you’ve reacted (to my infinite astonishment), more than to the information that I’ve transmitted.

Catching up with questions and comments

I wanted to just reply to a few comments and questions that have appeared here and on Twitter. I’m very gratified that so many people have clearly been thinking about this stuff.

I think we can and should generalise what I said about ski helmets to just about any realm of activity where they are “counted on” to provide protection. Construction hard-hats, bicycle helmets, hockey, Formula 1 pit crews, etc. The injury patterns almost certainly are different in each endeavour, and each therefore probably needs a different helmet. In general, we can’t expect the end user to do anything except have confidence in the equipment he (or she, that’s assumed in all my blog posts) chooses to use, or is obliged to use. That means that those who supply those helmets need to have a good idea of exactly what sort of injuries they need to mitigate. Clearly access to an appropriate level of protection has to be monetarily feasible. I chuckle to hear national-level rally drivers complain about a €2000 helmet (before going out and spending more than that on a set of tires! Helmets don’t make you fast!). I assume that a top of the line ski suit costs at least €800-1200. So that’s a constraint within which the manufacterers will have to work. They’re smart people. They’ll figure it out if the data gets generated.

Measuring g’s at the helmet with accelerometers is interesting, but there are severe enough problems with coupling to the head to make this data almost unusable in terms of BRAIN g’s. The DoD, and the FIA Institute, have been working on earpiece accelerometers for some time. These incorporate tiny 1 x 1 x 1 mm triaxial accelerometers into the part deepest into the ear canal. While this should theoretically give robust values for BRAIN g’s, that’s not happened yet. IRL has used earpiece accels for a while now, but I’m not sure they’re generating clinically useful data . . . yet.

Several people have sent me clippings concerning the effects of fish oil. Apparently someone “woke up” a comatose child using mega doses of fish oil. The explanations given were something like, well the brain is made up of fats, and so we give this good fat and it’s anti inflammatory too. The problem is that the person who administered this treatment published his results . . . on CNN. He should have published them in a peer-reviewed journal. Call me old-fashioned, but in terms of TREATING (not experimenting on) human beings, good quality evidence is the way to be guided, not what you saw last night on Dr. Sanjay Gupta’s show. That said, were I to be the close relative of a comatose head trauma patient, and were i to be  convinced that the risk profile of this kind of use of fish oil was acceptable, it is entirely possible that I’d be willing to have a go. But at the moment, let’s be clear, this is closer to ritual incantation than to medical science.

Lastly, something that’s been bothering me. A lot. As a doctor who practices pre-hospital medicine regularly.

Here goes: why was Michael brought to the hospital at Moutiers initially, and not to a neurosurgical centre? I am not trying to second guess (ok, just a bit) my colleagues who landed there on the 29th of December . . . BUT

  • reliable witnesses report to you that the victim hit his head
  • the victim’s helmet has been damaged in the impact
  • there’s blood on the snow
  • there is obvious signs of an open head injury
  • the victim is agitated (in any event his behaviour is not ENTIRELY normal)

Now I’m sorry, but it doesn’t take a doctor to put this together and figure out, “hey this person may have a head injury”.

Thing is, it is a general principle of pre-hospital medicine to take a patient to the closest APPROPRIATE facility. In a given Emergency Medical System’s territory, if this is applied “conservatively” it pretty much ALWAYS includes, for example paediatric cases and potential head injury. Thing is, there’s no neurosurgery at Moutiers. Why then was Michael brought there?

This question needs to be answered. As devastating as the injuries produced directly by the fall are, any delay in proper airway control and neurosurgical intervention cause further damage and must be minimised.

I raise this point simply because local protocols should be reviewed, and adjusted appropriately, in order to optimise the time it takes to get head-injured skiers cared for appropriately.

Some fascinating calculations, and one conclusion

Lots of people have asked me about the kind of forces involved in producing injuries similar to those Michael has suffered. It’s an interesting question, and after doing some calculations, it’s emphasised to me something that I think must be done relatively urgently. More of this later.

Let’s make a few assumptions as to baseline conditions. This means any results are at best approximations of the real world, but they allow us to “ballpark” the forces in question, and to perhaps compare with other mechanisms. And while I’m on the qualifiers, I’m SO not a physicist!

I’m assuming that the mechanism of injury is a near vertical fall onto the head, after Michael was “launched” by contact with a rock. I’ll assume his head was at 2.5 meters, not unreasonable for this kind of mechanism (and only slightly higher than one’s own height), that there was only a vertical component to his movement, and that he weighs 70 kg. This results in an energy of 1715 joules. Never mind the units for the moment – we’ll just generate some more energy data and then compare.

How about Felipe Massa’s accident? We know the spring weighed 800 gm (0.8 kg), and that Felipe was moving at 260 km/h (the spring is considered to have no horizontal velocity). This gives an energy of 2085 joules.

The same kind of calculation shows us that the bullet from a Kalashnikov (7.9 gm, muzzle velocity of 715 m/s, thanks Wikipedia!) has . . . 2019 joules!

To compare some other energies, let’s look at a soccer player heading the ball. Just to simplify, I’ll assume the player has no vertical speed when he heads the ball, and that the ball is falling from, say, 20 meters. This gives a “measly” 86 joules. Nothing, eh? (The actual value will be higher because of the player’s vertical momentum, and also if the ball falls from higher). Well how about this: there is a direct correlation between a the number of heads a soccer player has in his career and his cognitive function. So even this relatively tiny force, repeated many times, will likely damage a brain!

What about American football, where we read every day about cases of chronic traumatic encephalopathy (the damage done by years of hits)? Again, a few assumptions. Defensive lineman, 100 kg. Offensive lineman, 150 kg. Speed of each at impact? 1.2 meters/sec. What does this give? This gives us 180 joules combined. Again, doesn’t sound like much, but repeated over a career from high school, through college, to the pros, it seems often to result in very significant damage to the brain.

But back to the object of our concern. What explains the dramatic difference in outcomes between Michael and Felipe?

The obvious first (and perhaps only significant) answer is their helmets. Felipe was wearing the latest spec full face carbon kevlar racing helmet. Michael was wearing a . . . ski helmet.

Remember that force is not the only factor – we have to consider the area over which the force is spread. When a 70 kg man steps on your foot with his loafers, it hurts, but nowhere NEAR as much as when a 70 kg woman does the same with a stiletto heel. In one case, the force is spread over a much larger AREA, giving a lower pressure. And it’s pressure that actually does the damage. One of a helmet’s main roles is to distribute a force over a (much) larger area, dramatically reducing the pressures generated.

Now, the FIA Institute has done remarkable applied research in helmet design, and the helmet Felipe was wearing reflects that research. This helmet was designed specifically with very demanding requirements for impacts with objects having rounded edges as well as those having sharp edges, and equally for penetration resistance. These requirements were based on known mechanisms of injury in the sport concerned, and the levels of energy seen.

Ski helmets, on the other hand, are designed and homologated (WHEN they’re homologated) almost solely to prevent skull fractures. While this provides an easy method of evaluation in testing labs, we know that this has VERY little (if anything) to do with the actual mechanisms of brain injury. And unfortunately, Michael is a living demonstration of this.

Therefore, I’d like to throw a few ideas out there:

  • the Federations responsible for skiing, from recreational to competitive, should convene a working group of experts to look at the epidemiology of head injury in the sport
  • conclusions should be drawn about the kind of head protection likely to mitigate the injuries ACTUALLY SEEN
  • Jean Todt should offer the full resources of the FIA Institute (data, expertise, etc) to help design this helmet, to make it affordable, and to make sure it is used as widely as possible.

Michael’s injury is no more tragic than those of every patient who suffers severe head trauma. If, however, his public persona spurs action that goes on to significantly improve the safety of skiing, it will be another of his many remarkable accomplishments!