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.

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