options...pt with a temp of 103.7

Akulahawk said:
From what I've learned about it, I suspect that's the reason. It's effective on a HUGE range of organisms that it kind of fits into the "give it empirically" while we culture this and determine specific sensitivities and kill "it" with something specific.
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A lot of that stuff comes down to "fashion". Some docs prefer cefataxine (spelling??) some ceftriaxone. But certainly what you and vene have mentioned is why it is given early as part if the empirical treatment for SIRS/sepsis, followed by targeted ABs once the cultures are back.
 
Just want to interject here and inquire what your local protocol states regarding hyperthermia. Regardless of what you may want to do, and think is right for a particular situation, it is most important to adhere to your protocols.
 
well with regards to hyperthermia all depends if its pyrexia or related to enviroment. In NH protocols call for PO/PR acetominophen adult 325mg-650mg and pedi is 15mg/kg for fever in adult of pediatric.
 
I understand, and this is pretty standard across the board/states. I hadn't read all of the posted threads to this discussion. When I mentioned protocols, it was my intent to have that thread posted when some were discussing about the administration of cold NS as opposed to room temperature NS, etc, as well as applying cold packs. It seemed to be departing from what is normal treatment for a febrile patient. Thanks.
 
tah06090 said:
In NH protocols call for PO/PR acetominophen adult 325mg-650mg and pedi is 15mg/kg for fever in adult of pediatric.
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This might not be the case. I worked with a partner a few times who was a LPN at one of the lesser thought of NH in the service area, along with being an EMT-B, and she gave me a very good education on why NH do what they do. They aren't allowed to give meds they do not have prestanding orders for and have to call the facility doc for changes in vitals. Keep in mind that most of these docs are family pracs who supplement their income with the NH, and the same doc usually has multiple NHs that they only show up at once or twice a week. So, when they get a call from the NH the default answer is to punt to us.

This is not to justify the crap at NH that just makes you say WTF but it is something to consider when dealing with them.
 
I think they meant New Hampshire and not nursing home. :)
 
I agree with what some of the folks here have already said, it sounds like sepsis. You may want to investigate whether your protocols will allow you to give cooled saline in that situation, as it may not be indicated for anything other than environmental emergencies.

On a side note, a flight nurse I know recently told me that we may see a 10-20 mL/kg fluid bolus put in for patients meeting the septic criteria in the near future.
 
This turned out to be an interesting discussion...

To the OP. I would absolutely NOT give this pt cooled saline. As others have mentioned, this appears to be a metabolic issue and not an environmental one. We are allowed to give cooled saline post ROSC only. Not sure what your protocols are...

Sepsis is indeed topping my list of differentials here. He certainly has a plethora of potential origins. I'm also wondering about autonomic dysreflexia. While typically associated w/ SCIs above T6, it can be caused by other things as well. (recent CVA perhaps?) He certainly has a few of the s/s's.... Just throwing it out there....
 
Sam Adams said:
This turned out to be an interesting discussion...

To the OP. I would absolutely NOT give this pt cooled saline. As others have mentioned, this appears to be a metabolic issue and not an environmental one. We are allowed to give cooled saline post ROSC only. Not sure what your protocols are...

Sepsis is indeed topping my list of differentials here. He certainly has a plethora of potential origins. I'm also wondering about autonomic dysreflexia. While typically associated w/ SCIs above T6, it can be caused by other things as well. (recent CVA perhaps?) He certainly has a few of the s/s's.... Just throwing it out there....
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here's the question of the hour:

Since most bacteria multiply at physiologic temperature, would inducing hypothermia also clinically reduce reproduction of the microorganism as well as reduce metabolic demands of the patient?

That would be a good study.
 
and while I am thinkng about it,

Hypothermia also inhibits clotting which can preempt a DIC.

It may also decrease vascular permiability.
 
Veneficus said:
here's the question of the hour:

Since most bacteria multiply at physiologic temperature, would inducing hypothermia also clinically reduce reproduction of the microorganism as well as reduce metabolic demands of the patient?

That would be a good study.
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I'll see your hypothermically induced reduction of of bug proliferation, and raise you a reduction in the efficacy of his current other medications?
 
Sam Adams said:
I'll see your hypothermically induced reduction of of bug proliferation, and raise you a reduction in the efficacy of his current other medications?
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considering his condition, what do you see as his chances of survival with conventional therapy?

You might inhibit the ab that are already insufficent?

Inhibit a new ab? just give more.
 
Veneficus said:
and while I am thinkng about it,

Hypothermia also inhibits clotting which can preempt a DIC.

It may also decrease vascular permiability.
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Interesting.

Hypothermia also lowers the fibrillation threshold, right? With this guy's rate being through the roof already, I'd not want to think about the irritability that would show up if he dropped below 35.

Also, and I'm just thinking out loud here, with ten year old anectodal experience...could stalling the peripheral circulation by inducing hypothermia cause a compartment-syndrome like effect when he's rewarmed? All those metabolic products just hanging out, waiting for circulation to get going again?

Can you educate me on what this looks like in the OR, I know that our patients came back cooooold, especially from long surgeries with unstable periods. We warmed them immediately, and fought the cold because of the extra stress it put on the body, but now that I think of it, I can't remember what that stress resulted from, physiologically.
 
abckidsmom said:
Interesting.

Hypothermia also lowers the fibrillation threshold, right? With this guy's rate being through the roof already, I'd not want to think about the irritability that would show up if he dropped below 35.

Also, and I'm just thinking out loud here, with ten year old anectodal experience...could stalling the peripheral circulation by inducing hypothermia cause a compartment-syndrome like effect when he's rewarmed? All those metabolic products just hanging out, waiting for circulation to get going again?

Can you educate me on what this looks like in the OR, I know that our patients came back cooooold, especially from long surgeries with unstable periods. We warmed them immediately, and fought the cold because of the extra stress it put on the body, but now that I think of it, I can't remember what that stress resulted from, physiologically.
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There is a long held theory about hypothermia being part of a deadly triad in traumatic injury, like surgery, and many of the studies and observations are beyond reproach.

However, much of that was discovered before theraputic hypothermia. We know it has a benefit in certain types of trauma. We know it helps post arrest.

So my question then becomes can the very mechanisms that make hypothermia so deadly in bleeding with an open wound, be used to beneficial purposes to prevent the complications of sepsis?

Since I just thought of it on the spur of the moment, I really don't have a lot of answers.

http://en.wikipedia.org/wiki/Trauma_triad_of_death
 
Interesting question vene. Excuse my rambling, this is largely stream of consciousness here: At what point would we expect to see suppression of the biological functions of bacteria that would meaningfully inhibit their activities, as opposed in inhibition of normal cellular function that leads to worse outcome. If cold is (hypothetically) bacteriocidal or even causes bacteriostasis, why do we not see an improvement or even plateau in the condition of patients in cold shock with temperatures of 32C and the like who are also recieving aggressive supportive care that would hopefully overcome the detrimental effects of hypothermia?

Petey0397 said:
On a side note, a flight nurse I know recently told me that we may see a 10-20 mL/kg fluid bolus put in for patients meeting the septic criteria in the near future.
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Really? Why so aggressive with the fluids?...
 
Petey0397 said:
On a side note, a flight nurse I know recently told me that we may see a 10-20 mL/kg fluid bolus put in for patients meeting the septic criteria in the near future.
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Sorry, I was being facetious in my last post. 10-20mls/kg of crystalloid in a septic patient would barely even touch the sides on it's way through. These patients (particularly septic shock patients) are often getting 40ml, 60ml, 80ml/kg and more of crystalloids as well as colloids and pressors and are still struggling to maintain a CVP of 2mmHg (although there is also debate as to how useful measurement of CVP is in septic patients)
 
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