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.