Delaying Fluid Resuscitation

Ridryder911

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Metabolic acidosis, due to the build up of lactic acid?

Very Good! Lactic Acidosis is one of the first things we want to identify in trauma patients, by running a lactic acid profile. Now research what the level of pH Normal Saline and Lactated Ringers are.. and is this really helping the patient?

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csykes

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Considering in the most field settings we have no way to measure arterial gas pH, we can only predict that it is occuring. Specific events heightening our suspsicion would be crush injuries, burns, long down time codes, and increased ETCO2 measurements. Our best course of field treatment is going to be altering the respiratory acidocisis, thereby decreasing the amount of H2CO3 in the body through increased ventilaitons. Na2(HCO3)2 or Sodium Bicarb is the drug of choice for decreasing metabolic acidosis. Rhabdomylsis is a big cause of this metabolic acidosis in the trauma patient and from my experience has been treated by 100mEq of bicarb in 1L NS over and hour or two. The 3 ways to correct acidosis is 1)respiratory 2)bicarb buffer system 3)proton filtration through kidneys.
 

Veneficus

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Considering in the most field settings we have no way to measure arterial gas pH, we can only predict that it is occuring. Specific events heightening our suspsicion would be crush injuries, burns, long down time codes, and increased ETCO2 measurements. Our best course of field treatment is going to be altering the respiratory acidocisis, thereby decreasing the amount of H2CO3 in the body through increased ventilaitons. Na2(HCO3)2 or Sodium Bicarb is the drug of choice for decreasing metabolic acidosis. Rhabdomylsis is a big cause of this metabolic acidosis in the trauma patient and from my experience has been treated by 100mEq of bicarb in 1L NS over and hour or two. The 3 ways to correct acidosis is 1)respiratory 2)bicarb buffer system 3)proton filtration through kidneys.

Just some perspective on field measurements and treatments for the new people.

The reason we measure lactate is because we understand how it correlates to ATP production in a cell. (which we cannot measure) For specific treatments, we like specific measurements, but cellular or systemic PH is not the only end game.(but is one of the ways to denature proteins we need to survive) We add oxygen hoping to trade it for CO2, which would mean the TCA cycle in cells is intact. Neuro tissue can only live long term from aerobic metabolism, cardiac tissue requires the energy from fatty acids, which produces more than 5 times the ATP of glycolysis. All of this relies on mitochondrial enzymes, which after being in anaerobic metabolism can release cytochrome C which starts apoptotic cascades causing cellular death. Furthermore many of the treatments in EMS and in the ED do not address liver function, which converts lactate to back to pyruvate which can reduce systemic PH and provide a way to keep TCA working so that muscle breakdown is limited. Moreover, not only do amino acid chains alter PH, they attach to each other and can form clots in nephron tubes and vascular beds.

This is why I keep professing that the idea of current “field” treatments may not be doing as much as we hope in helping patients. The treatments assume the body is still capable of compensating until all the causes can be addressed, but does not address anything not relying on systemic circulation. (like the liver, which only gets 25% of its requirements through systemic circulation) so we may be losing multiple organs in our zeal to supply heart, brain, and kidneys but nothing else.

In a severly injured person, you can just assume acidosis. But even then buffers may not help.
 

41 Duck

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Okay. I've read on with interest, and do completely understand what you, Rid, are saying with regards to acidosis in the trauma PT, and fluid recussitation. I also get the bit Veneficus mentioned about losing peripheral organs to preserve the heart and brain.

I'm not a paragod student. Just some dumb mick out in East Boonies, PA, trying to keep passing class and surviving my hospital clinicals long enough to be a street medic next November.

To answer Rid: 5.5 and 6.6, respectively--and adding lactate to someone in lactic -based acidosis just seems a wee bit wrong to me. But now... given that which we have to work, what do you suggest?

Let's say you guys are given The Golden Pen to write Trauma protocols. How would they read? Would you be including, perhaps, bicarb, for acidosis more often? The only place I can think of it being part of our trauma protocols out here is for crush syndrome prior to extrication. In your opinion, should this be utilized more often? Something else?

I realize the above could come across as antagonistic--and I hope it's not taken that way. I am, honestly, very interested in learning what someone who forgot more than I learned would do, if they were given carte blanche.

Thanks.


Later!

--Coop
 

Ridryder911

EMS Guru
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The paragod statement was just a joke.

Now, in regards to acidity of the NSS you are right. Part of the problem of fluid resuscitation as well. Do we really want to increase acidosis? Also remember, the first half hour is when the regulatory systems is adjusting and taking action.

Alternatives? Something we need to continue researching. As well, although Hartman's solution (RL) is also acidotic it does have some buffer qualities that is helpful in the initial treatment. Maybe more a volume expander than fluids itself?

I agree with saline as a secondary or alternative line or as a lock to administer blood through.

I suggest listening to shock treatment from PHTLS podcast, some interesting discussion and facts.

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Veneficus

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Let's say you guys are given The Golden Pen to write Trauma protocols. How would they read?

It is not my golden pen which is a danger; it is my poison quill ;)

The one word answer to a trauma protocol I think is: “depends.”
There is a lot that must be taken into account, so I think it needs to be many protocols, not one.

If you want a real teaser, in a multisystem trauma patient, where there is a brain injury as part, the treatments for the brain and the rest of the body are diametrically opposed. The best answer I have gotten from minds greater than my own is “It becomes a balancing act and you have to use your clinical judgment”

So you probably need a protocol for ortho trauma. A separate for trauma with uncontrolled hemorrhage, with controlled or controllable hemorrhage, head injury, spinal injury, as well as treatments based on how long the patient has been or will be without a hospital.

What’s more is this approach where one size does not fit all has to be reconciled in training and education. But without spending the time it would take to write all this out in detail (so a few details will be missing) it would look something like:

Ortho injuries: assess extent of injury (if no MSP attempt to realign), immobilize, control pain, transport

Hypothermic therapy if available for all of these:

Isolated head injury: Assess for deficits, maintain airway, 2 IVs, maintain SBP ~120 or greater, 02, transport, hyperventilate only when about to go to surgery.

Uncontrolled hemorrhage: attempt to control such, maintain airway, 02, IV if there is time or (by some miracle) you carry blood. Transport

Controlled/no hemorrhage: maintain airway, 02, start IV, depending on severity of injury fluid, attempt to maintain bp >100 systolic, possibly furosimide, possibly bi carb. Depending on extent of muscle damage.

Spinal impairment, or suspect of: c-collar, maintain airway, o2, gently move patient to stretcher, preferably with a scoop stretcher, unsecured board, or full body vacuum splint. Transport. If no bleeding attempt to maintain bp >100 systolic.

I should add decompress pneumo, pericardial centisis, generally deal with ABC issues.

That is just off the top of my head.

The only place I can think of it(sodium bicarb) being part of our trauma protocols out here is for crush syndrome prior to extrication.

I think I would just teach medics a bit more anatomy and give them a #10 scalpel. But some bicarb is a good idea too.
 
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