Kevin Everett: Science 1, Debilitating Injury 0

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This obviously isn't the neurosurgery forum, but what the hell.

As anybody who pays any attention to pro football knows, Kevin Everett had what was supposed to be a "catastrophic" neck injury at the C3-C4 level while making a tackle on Sunday. Prelim reports sounded all kinds of bad, and while he went immediately to surgery, his neurosurgeon as much as said he'd have a dismal chance of ever walking again.

Cut to today- apparently he's moving all extremities (how much isn't clear), and with minimal swelling on MRI. Like, wow. Then come to find out the reason for this apparent miracle:

From ESPN.com: http://sports.espn.go.com/nfl/news/story?id=3014742

"I don't know if I would call it a miracle. I would call it a spectacular example of what people can do," Green said. "To me, it's like putting the first man on the moon or splitting the atom. We've shown that if the right treatment is given to people who have a catastrophic injury that they could walk away from it."

Green said the key was the quick action taken by Cappuccino to run an ice-cold saline solution through Everett's system that put the player in a hypothermic state. Doctors at the Miami Project have demonstrated in their laboratories that such action significantly decreases the damage to the spinal cord due to swelling and movement.

"We've been doing a protocol on humans and having similar experiences for many months now," Green said. "But this is the first time I'm aware of that the doctor was with the patient when he was injured and the hypothermia was started within minutes of the injury. We know the earlier it's started, the better."

I mean, wow. This is fricking earth-shattering stuff IMO. We've all read about the likely benefits on survival with hypothermia in acute MI scenarios, but I had no idea this was being looked at with acute spinal cord injuries. It sounds like Everett was probably the earliest hypothermia intervention they've been able to accomplish, and you really can't argue with the results.

I suppose it's possible that his injury was such that he would have had this result without the hypothermia, and they just overcalled the extent of it, but that just seems much less likely given how experienced these guys are with these injuries. He wouldn't have given that initial prognosis without good reason.

I'll say it again because it's so goddamn amazing: HOLY HYPOTHERMIA, BATMAN. If the difference between this guy living a potentially completely normal life versus spending the rest of his days as a quad was something as easy to administer as a quick cold saline infusion, then bravo very much to the guys behind this research. The implications are just mind-boggling when you consider the outcome differences. Very well played, sirs. Well played indeed.

I may be completely over-reacting here, but I don't think so.
 
Golly, I hope they're right.

Earlier studies with apoptotic-arrest therapies, such as hypothermia, worked quite well acutely but suffered problems in the delayed phase. That is, the cells didn't die while cold, but you have to wake them up at some point. Once warm, the apoptotic pathway continues leading to cell death.

This may also have been due to localized cord edema resolving.
 
True- but the effects here aren't from anti-apoptosis as they are in the post-MI pts, but rather from the acute anti-inflammatory effect of hypothermia that presumably prevents the damage that the inflammation around the cord would otherwise have caused within the first few hours post-injury.
 
Correct me if I'm wrong, but I thought the problem with spinal cord injuries was that the cord pathways were CUT. As in, no more axons traveling where they are supposed to go. Edema around the cord causes temporary effects (ie: blast effect in gunshot wounds near the cord), but never caused the permanent paralysis you saw in cord transections.

I can be somewhat skeptical at times, and I see this as being doctors trying to play up what was basically a missed diagnosis from the start. Had he transected his cord no amount of cold saline would put it back together again.
 
His cord was not transected as far as I can tell. He was put on the stretcher without any sort of ventilatory assistance needed. If his C3-4 cord was transected he would not have been breathing on his own. C345 keeps the diaphragm alive.
 
Clearly transection was never a consideration, given that he maintained tactile sensation throughout his body and was still breathing. It sounds like the most likely mechanism given his motor deficit and the surgery he had was a burst fracture of C3 or C4 with impingement on the anterior cord. The hypothermia would have presumably minimized any further inflammation from the impingement that would then have gone on to become an irreversable cord injury.

I just have a hard time believing that a neurosurgeon good enough to be a consultant to a pro football team would have called this injury "catastrophic" without reason and experience with whatever type of injury he had, especially considering he said this post-op after he went in and saw for himself what he was dealing with.

Regardless, the bottom line is that it's awesome this guy will probably walk again, and he's a frigging lucky guy for that no matter if the hypothermia made a difference or not.

And now back to your regularly scheduled "I have a 240 Step 1 but I'm only in the upper 1/3rd of my class, do I have any shot at all?!?!?!" threads.
 
Correct me if I'm wrong, but I thought the problem with spinal cord injuries was that the cord pathways were CUT. As in, no more axons traveling where they are supposed to go. Edema around the cord causes temporary effects (ie: blast effect in gunshot wounds near the cord), but never caused the permanent paralysis you saw in cord transections.

Not that simple. Edema in closed spaces such as skull and spinal canal can lead to ischemia and permanently worsened outcomes. That is why so many neuroprotective schemes target secondary injury resulting from inflammation and the obligatory edema (e.g. hypothermia, steroids, glucose control, barbiturates). Sometimes there is not much that can be done about the initial neurologic insult but we can always take steps to minimize secondary injury. This case is an example.
 
Didn't see the replay of the injury, but from what it sounds like, it's central cord syndrome, even if he didn't have a classical injury via hyperextension.

Yes, he may be able to walk; but what function will he have in his arms? Another concern: how much sacral root function was spared? That's gonna be the kicker.
 
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