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A try at some mental gymnastics. Suspension trauma.


DwayneEMTP

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Treating life threatening hyperkalemia involves a three prong approach:

1) Stabilise the cell membrane potential

2) Shift Potassium into the cells

3) Eliminate the Potassium

Membrane stabilisation is the immediate treatment in life threatening hyperkalaemia. Sodium bicarbonate is not necessarily the front line, stop-gap intervention.

I am not completely sure that rhabdo is present in this guy, nor is it going to be present in every suspension type injury. Rhabdo is the result of massive tissue (muscle) damage leading to massive numbers of cells rupturing and releasing their contents, Potassium and myoglobin among the various substances.

While acidosis alone will cause a K+/H+ exchange to occur, the Potassium imbalance of rhabdo has additional pathophysiology at play.

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...I am not completely sure that rhabdo is present in this guy, nor is it going to be present in every suspension type injury...

This is kind of the crux of my interest in this part of the conversation. A Dr. gave a speech in 1972 (according to multiple sources that can be refound if they are important to anyone here) at a medical conference explaining his theory that Rahbdo should be present in these injuries, and it was accepted from that point on in nearly every circle that had interest in such things until, as often happens, it was simply accepted, and taught, as well proved fact, despite there being no studies validating it.

I was taught that particularly if a pt has become altered secondary to hanging in a harness sedately, that you lower him into a sitting position, leave the harness in place, transport sitting up, and be prepared to mitigate cardiac arrhythmias with sodium bicarb if necessary. (The reason I've pounded on delivery methods and amounts is that I was never, to the best of my knowledge, taught that specifically, just that I might consider using it.)

But it turns out that Rhabdo is almost never, and possibly never, at least in the type of patient described without associated fall trauma, present in these patients. That most of the morbidity and mortality comes from leaving them sitting, allowing the cerebral hyperperfusion secondary to the blood pooling to continue.

I actually got stuck on this path after reading a Wiki article on the subject where the incredibly poorly written article explained that the patient should be lay down and treated the same as any other patient altered secondary to hypoperfusion. I'd intended to make the comment that "This article is so misinformed as to be dangerous." but wanted to be able to source my opinion....then found out that I couldn't.

One of the articles used surgeries on large muscle extremities as an example. They mention lower extremity surguries where the leg has been tourniqueted (not sure if that's a word) for sometimes four or five hours, with the associated muscle damage and release of cellular contents from the proceedure, yet, the article claims, though it's monitored, rarely is mitigation of pH and/or electrolyte pathologies necessary. (Though, the one or two vids I've seen of these types of surgeries they wrapped the leg from bottom to top very tightly with gauze to force as much blood out as possible before placing the tourniquet, so I'm not sure if this example clearly applies without relevant volumes of blood pooling to reenter circulation??)

So the recommendation seems to be for prehospital personnel, at least in the UK and Austraila (the places most often returned in searches when I'm in PNG) that these patients be treated as any other pt believed altered due to hypoperfusion...A, B, Cs...

Again, my apologies for the lack of sources. I'd not really intended to post this when I started looking into it, and then, as I'm sure most understand it was an exercise in 'stream of hyperlink' research, so I didn't keep track of when or where I found the things mentioned and won't be at all offended if the comments are discounted on that basis. I've just not had time to try and retrace my steps here.

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