Ceci est une copie de l’article publié par Autosport ce jeudi 09 janvier 2014. Je ne le publie ici que parce qu‘Autosport n’est pas disponible en France. Si vous estimez que je dois le retirer merci de me le signaler en laissant un commentaire….
Gary Hartstein – The inside line -
Ex-F1 medical delegate – and consultant anaesthetist and A&E physician – analyses reports of Michael Schumacher’s condition
Let’s take a look at what’s happened to Michael
Schumacher, from his fall until roughly now. It goes
without saying that this is based on what we’ve been
told at the press conferences, viewed and interpreted
through my eyes. I will not speculate, but will rather read
between the caring physicians’ lines and put this into the
context of the treatment of severely head-injured patients.
It’s useful to think of the impact against the rock
as having done two things: it essentially immediately
created a series of severe lesions, and it set into motion
processes that, left to themselves, would aggravate the
damage already done.
What about the initial lesions? There were probably at
least four types of injury produced by the fall.
The first is formation of haematomas. Torn and
damaged blood vessels let blood escape in sufficient
quantity to coalesce. They are dangerous both because
they are markers of severe impact as well as because
they cause the intracranial pressure (ICP) to rise. We’ve
been told that Michael had a right-sided extradural
haematoma (between the skull and the dura, a membrane
surrounding the brain) that was evacuated surgically a
week last Sunday, and a series of intracerebral (within
the brain tissue itself) haematomas. One of these, on the
left, was evacuated last Monday, but there are several
others, located on the left, on the right and in the centre.
The second type of injury is contusions. These are
bruises, just like when you bang your arm or leg. Tiny
quantities of blood seep from the vessels, but not
enough to collect. This gives that black-and-blue
look. There’s also swelling of course, which adds
to the ICP increase caused by the haematomas.
Third is the possibility of damage to the long ‘cables’
in the brain. Injury to these axons is harder to see
with modern imagery, but is often associated with
poor neurological outcome.
Last, I have heard insistent stories of damage to one
of the four arteries feeding the brain. Even if true, the
significance of this is hard to assess, as most people have
extensive connections between the four arteries, allowing
flow through one to compensate for blockages in another.
What about the vicious circles I alluded to above?
The most important revolves around the ICP. Increased
ICP compresses the tiny blood vessels nourishing the
brain. The problem is, when the brain isn’t receiving
enough blood, what do you think it does? Right –
it swells. This aggravates the already high ICP, and
the already low blood flow.
Taking care of severely head-injured patients involves
rigorous adherence to a few principles. Basically, the brain
needs to consistently receive adequate amounts of oxygen
and nutrients. For this to happen, the air passages are
maintained open and secure by a tube placed in the
windpipe. Oxygenation and ventilation are provided by
sophisticated ventilators, and adjusted to values as close
to normal as possible. In order to ensure proper brain
blood flow, it is urgent to control elevated ICP.
The first step in controlling high ICP was done on
the Sunday and Monday after Schumacher’s accident.
The surgically accessible haematomas were evacuated.
In addition, the bone flaps opened by the surgeon
weren’t closed, allowing the brain to physically
swell a bit before the pressure rises.
It turns out that cooling the patient just a few degrees
can help make sure that energy delivery is adequate. This
is because cooling slows the brain’s metabolism. That
means that any given level of oxygen and nutrient delivery
is more likely to be sufficient for the brain’s needs.
Hypothermia is also very effective against elevated ICP.
It’s also important to understand what is meant by,
and the role of, the ‘medically-induced coma’.
I mentioned controlling the airway with a tube in the
trachea, controlling breathing with a ventilator and
reducing body temperature. Now, realistically you just
can’t do this to a patient, even a severely head-injured
patient (especially not a head-injured patient!) without
anaesthetising them. So all these patients are put to sleep.
This also helps ensure that the patient doesn’t shiver
during the period of hypothermia (usually 48-72 hours).
If despite all the above the ICP stays elevated, the
anaesthesia is deepened significantly. This aims at
temporarily abolishing electric activity in the brain,
in order that all available energy be used for vital
cellular maintenance, not ‘superfluous’ activity.
The future? A long, long road. Months at least. Short
term, the anaesthetic needs to be lightened when the
ICP is normal and stable. That’s the next big step.