Gave a pt an entire bag of IV fluid the other day

medichopeful said:
Personally if they're not perfusing their peripheries well, I just like to go straight to pressors. Jump the gun a little, you know, mix things up. Keep it interesting.
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A warm bag of dobutamine to hold...best of both worlds...
 
Agreed with @medichopeful regarding "liberal" fluid boluses in the septic patient. Oftentimes the sequence of events leads to interstitial fluid shifts in these patients bed confined in an ICU TMK. Ask any ICU nurse and I am sure they can attest to the nightmare that these patients can become.

Where we fail with paramedic students is all too often we only teach a "treat what we see" method, and some people can't think beyond that; that's a huge problem for another thread if anyone wants to start an actual discussion on it.

I think a good safe 1-2 liters of fluids before moving on to pressors is practical in the (extended transport) prehospital environment, but perhaps I'm just more conservative.

When I think aggressiveness of fluid delivery I often think of the DKA, or HHNK patient.
 
VentMonkey said:
When I think aggressiveness of fluid delivery I often think of the DKA
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We just had this discussion in class, forgot to add it to my other post.
 
StCEMT said:
Isn't the idea behind this increasing volume to dilute concentration?
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Thats how it was explained to me in the case of DKA. Aggressive fluids to dilute blood glucose.
 
StCEMT said:
Isn't the idea behind this increasing volume to dilute concentration?
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CALEMT said:
Thats how it was explained to me in the case of DKA. Aggressive fluids to dilute blood glucose.
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There's also something to be said about renal perfusion. In the prehospital setting, sure dilute away, but remember these patients are often severely dehydrated and dry as a bone (think "3 P's") as they often have symptoms such as increased N/V, and are metabolically acidotic.

In the hospital they're usually placed on maintenance fluids as well as insulin with a D5W gtt as sudden drops in their glucose is bad, especially in pediatrics (our Central Valley peds ED has a whole protocol for it); it leaves them susceptible to cerebral edema.

Listen to Bauer's podcast I posted in another thread, he talks about this exact patient population in the critical care transport environment.
 
CALEMT said:
Thats how it was explained to me in the case of DKA. Aggressive fluids to dilute blood glucose.
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Yea, didn't know if there is ever a time we fill the tank and just let the body help remove stuff through urine or if dilution was the main idea.
 
Well mimicking vents post the body is in overdrive trying to get the excess glucose out via the renal and respiratory system. The body compensates with increased breathing and increased renal output due to the acidosis. The kidneys care cranked up to level 10 and can't sustain that for X amount of time, so renal failure is a option. Which is why you dump fluids in so you can try to dilute the glucose and you can replace volume/ hydrate to try to take the workload off the kidneys. I can go further in depth, but this summarization is how it was explained during the endocrine lecture and makes the most sense for me. So I guess its a little of both St.
 
VentMonkey said:
There's also something to be said about renal perfusion. In the prehospital setting, sure dilute away, but remember these patients are often severely dehydrated and dry as a bone (think "3 P's") as they often have symptoms such as increased N/V, and are metabolically acidotic.

In the hospital they're usually placed on maintenance fluids as well as insulin with a D5W gtt as sudden drops in their glucose is bad, especially in pediatrics (our Central Valley peds ED has a whole protocol for it); it leaves them susceptible to cerebral edema.

Listen to Bauer's podcast I posted in another thread, he talks about this exact patient population in the critical care transport environment.
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What? You mean we should actually pay attention to signs and symptoms like polyphagia, polydipsia, and polyuria? What is this witchcraft. I just drive
 
CALEMT said:
Thats how it was explained to me in the case of DKA. Aggressive fluids to dilute blood glucose.
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Kind of. DKA patients are also absurdly dehydrated, leading to the need to rehydrate them. But it has to be done carefully, because of all the fluid/electrolyte shifts.
 
medichopeful said:
Sepsis is a fine balance. Overly aggressive fluid resuscitation in septic patients can actually be detrimental.

In this scenario, nothing was infused. He used a warm bag of fluids as a warm object. Smart idea, but misleading post.
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I read something interesting recently regarding fluid resuscitation in septic patients, it made even have been on here. It was a number of "myths" that the Surviving Sepsis campaign has in their guidelines and one of them was aggressive fluid resus for everyone. We do 20mL/kg instead of 30 and start pressers really early. Like the same time we start the fluids early.


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Handsome Robb said:
I read something interesting recently regarding fluid resuscitation in septic patients, it made even have been on here. It was a number of "myths" that the Surviving Sepsis campaign has in their guidelines and one of them was aggressive fluid resus for everyone. We do 20mL/kg instead of 30 and start pressers really early. Like the same time we start the fluids early.


Sent from my iPhone using Tapatalk
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Wasn't this part of an emcrit podcast on sepsis?
 
I chuckled
 
CALEMT said:
Well mimicking vents post the body is in overdrive trying to get the excess glucose out via the renal and respiratory system. The body compensates with increased breathing and increased renal output due to the acidosis. The kidneys care cranked up to level 10 and can't sustain that for X amount of time, so renal failure is a option. Which is why you dump fluids in so you can try to dilute the glucose and you can replace volume/ hydrate to try to take the workload off the kidneys. I can go further in depth, but this summarization is how it was explained during the endocrine lecture and makes the most sense for me. So I guess its a little of both St.
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Pretty much correct. The respiratory system doesn't blow off any glucose, however.

The issue with DKA is that the body can't use sugar for energy (due to the fact that insulin isn't there). The patient will continue to eat sugar, however. The body, in place of sugar, will break down fats for energy, which leads to the presence of ketones in the blood. These ketones lead to a metabolic acidosis (hence the name, "diabetic ketoacidosis"). The body, sensing this imbalance in pH, attempts to compensate by blowing off excess CO2 (here is where you get Kussmaul's respirations). That's why you should avoid RSIing a patient in profound DKA. If they can't hyperventilate, they'll become even more acidotic and you'll be working an acidotic arrest. Bad news bears.

When it comes down to the renal side, you're correct that renal failure is an option. My understanding is that the mechanism behind the excessive urination is that in the renal system, the body will try to eliminate ketones and glucose through urinary excretion. Glucose and ketones pull fluid with them when they are eliminated by the kidneys (oncotic pressure if I remember correctly?). This is where you get the polyuria and, subsequently, polydipsia. Electrolyte imbalances can then follow, which can be compounded by nausea and vomiting. DKA patients are sick and critically ill.

Treatment of these patients involves fluid resuscitation/rehydration, and correction of electrolyte imbalances. Insulin drips are started as well, sometimes only after fluid resuscitation is done. Insulin drips and fluids are continued until the BGL reaches a certain level, then sugar (for example, D5W) is added to the fluids so the insulin drip can continue so that the anion gap can close. Once the anion gap has closed and sugars are under control, the patient should be switched to sliding scale insulin.

Management of these patients isn't necessarily easy, and they need to be monitored very closely. Electrolytes (especially K+) need to be monitored throughout treatment (remember, insulin drips lower potassium levels, and may lead to hypokalemia). The whole process is actually fascinating.
 
Handsome Robb said:
I read something interesting recently regarding fluid resuscitation in septic patients, it made even have been on here. It was a number of "myths" that the Surviving Sepsis campaign has in their guidelines and one of them was aggressive fluid resus for everyone. We do 20mL/kg instead of 30 and start pressers really early. Like the same time we start the fluids early.


Sent from my iPhone using Tapatalk
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I think StCEMT is right. I believe that was in an EMCrit podcast.

I also saw an interesting article on pressors in sepsis recently (possibly on EMCrit). Although norepi is a great drug for sepsis, it isn't always the best. I can't find the page, however.
 
VentMonkey said:
Agreed with @medichopeful regarding "liberal" fluid boluses in the septic patient. Oftentimes the sequence of events leads to interstitial fluid shifts in these patients bed confined in an ICU TMK. Ask any ICU nurse and I am sure they can attest to the nightmare that these patients can become.

Where we fail with paramedic students is all too often we only teach a "treat what we see" method, and some people can't think beyond that; that's a huge problem for another thread if anyone wants to start an actual discussion on it.
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With enough fluids, I swear they start 4th and 5th spacing. They seriously blow up like a balloon, which may then lead to issues with weaning, which leads to badness.

I'm going to start a discussion on the "treat what we see" issue that you pointed out. I'd be interested to see what people's thoughts are on the issue.
 
Tigger said:
Wouldn't a hot pack have worked much better?
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We don't carry hot packs, just the chemical cold packs. Our truck is the only one in our service that happens to have a warming drawer, so the quickest way to warm up the pts extremities was to use a warm bag of fluid. Winter time, we also started keeping a bag of d10 in there, as one of the medics on our truck had issues pushing air temp d10 one day.
 
Dennhop said:
We don't carry hot packs, just the chemical cold packs. Our truck is the only one in our service that happens to have a warming drawer, so the quickest way to warm up the pts extremities was to use a warm bag of fluid. Winter time, we also started keeping a bag of d10 in there, as one of the medics on our truck had issues pushing air temp d10 one day.
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How would you push D10? Must be a real bear to push room temp D50 then.
 
medichopeful said:
Pretty much correct. The respiratory system doesn't blow off any glucose, however.

The issue with DKA is that the body can't use sugar for energy (due to the fact that insulin isn't there). The patient will continue to eat sugar, however. The body, in place of sugar, will break down fats for energy, which leads to the presence of ketones in the blood. These ketones lead to a metabolic acidosis (hence the name, "diabetic ketoacidosis"). The body, sensing this imbalance in pH, attempts to compensate by blowing off excess CO2 (here is where you get Kussmaul's respirations). That's why you should avoid RSIing a patient in profound DKA. If they can't hyperventilate, they'll become even more acidotic and you'll be working an acidotic arrest. Bad news bears.

When it comes down to the renal side, you're correct that renal failure is an option. My understanding is that the mechanism behind the excessive urination is that in the renal system, the body will try to eliminate ketones and glucose through urinary excretion. Glucose and ketones pull fluid with them when they are eliminated by the kidneys (oncotic pressure if I remember correctly?). This is where you get the polyuria and, subsequently, polydipsia. Electrolyte imbalances can then follow, which can be compounded by nausea and vomiting. DKA patients are sick and critically ill.

Treatment of these patients involves fluid resuscitation/rehydration, and correction of electrolyte imbalances. Insulin drips are started as well, sometimes only after fluid resuscitation is done. Insulin drips and fluids are continued until the BGL reaches a certain level, then sugar (for example, D5W) is added to the fluids so the insulin drip can continue so that the anion gap can close. Once the anion gap has closed and sugars are under control, the patient should be switched to sliding scale insulin.

Management of these patients isn't necessarily easy, and they need to be monitored very closely. Electrolytes (especially K+) need to be monitored throughout treatment (remember, insulin drips lower potassium levels, and may lead to hypokalemia). The whole process is actually fascinating.
Click to expand...

Was re-reading this thread, and realized I forgot to mention that long-acting insulin might be added in as well.
 
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