Lasix, Cr, and IVF

[LouisianaDoctor]

Hi all,

I have a few questions regarding Lasix. I understand the indications and how it works. I know that IV Lasix is twice as "potent" as PO Lasix, and I know several ways to figure out a initial dose of Lasix in the inpatient setting. However, I have many questions about its use in this setting.

1. One thing I don't understand is how we should interpret BUN/Cr in these patients. For example, if I'm giving a patient Lasix and their BUN and Cr are rising, what is this telling me? Is this Lasix damaging the kidneys, or is it telling me that I am removing fluids from the patient and things are "concentrating" (ie, the same concentration of BUN, but in a smaller volume.) Is this when I should look for a > 20:1 BUN/Cr ratio?

2. When administering IV Lasix, when do you make the switch back to PO? I've been told that you can switch back to PO if the patient is symptomatically improving, or if they experience a bump in their Cr. And how would you convert the dose back to PO? Would you have to double it?

3. What is the difference between giving someone, for example, 80 mg of Lasix IV BID, as opposed to a 20 mg/hr drip? I understand the quantity given will be different, of course, but why would I pick a drip?

Thank you kindly for any insight.

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[PMPMD]

Hi all,

I have a few questions regarding Lasix. I understand the indications and how it works. I know that IV Lasix is twice as "potent" as PO Lasix, and I know several ways to figure out a initial dose of Lasix in the inpatient setting. However, I have many questions about its use in this setting.

1. One thing I don't understand is how we should interpret BUN/Cr in these patients. For example, if I'm giving a patient Lasix and their BUN and Cr are rising, what is this telling me? Is this Lasix damaging the kidneys, or is it telling me that I am removing fluids from the patient and things are "concentrating" (ie, the same concentration of BUN, but in a smaller volume.) Is this when I should look for a > 20:1 BUN/Cr ratio?

2. When administering IV Lasix, when do you make the switch back to PO? I've been told that you can switch back to PO if the patient is symptomatically improving, or if they experience a bump in their Cr. And how would you convert the dose back to PO? Would you have to double it?

3. What is the difference between giving someone, for example, 80 mg of Lasix IV BID, as opposed to a 20 mg/hr drip? I understand the quantity given will be different, of course, but why would I pick a drip?

Thank you kindly for any insight.

1. I will limit my answer to acute kidney injury (AKI), as I'm a critical care fellow and that's where most of my experience lies. The evidence regarding the use of loop diuretics in AKI is inconsistent. The bulk of the evidence shows there is no effect either way on the course of AKI with loop diuretics. Again, in the specific case of AKI, we administer diuretics not to alter the course of AKI but rather to manage the extra-renal complications, for example, pulmonary edema.

2. One of the reasons to choose IV vs PO lasix has to do with bowel edema (more of an issue in right-sided heart failure than AKI.) These patients would have to be diuresed well before they will absorb PO lasix from the GIT.

3. Typically, someone will be placed on a continuous infusion if they don't respond to intermittent bolus doses. Keep in mind, the loop diuretic has to be secreted into the tubule to work, so larger doses are needed when GFR is lower.

 

[CaptainSSO]

1. I will limit my answer to acute kidney injury (AKI), as I'm a critical care fellow and that's where most of my experience lies. The evidence regarding the use of loop diuretics in AKI is inconsistent. The bulk of the evidence shows there is no effect either way on the course of AKI with loop diuretics. Again, in the specific case of AKI, we administer diuretics not to alter the course of AKI but rather to manage the extra-renal complications, for example, pulmonary edema.

2. One of the reasons to choose IV vs PO lasix has to do with bowel edema (more of an issue in right-sided heart failure than AKI.) These patients would have to be diuresed well before they will absorb PO lasix from the GIT.

3. Typically, someone will be placed on a continuous infusion if they don't respond to intermittent bolus doses. Keep in mind, the loop diuretic has to be secreted into the tubule to work, so larger doses are needed when GFR is lower.

Why does furosemide often cause hypokalemia?

My understanding is that it inhibits the NKCC2 co-transporter in the thick ascending limb of the loop of Henle, so is it the reduced K+ reabsorption here that leads to the hypokalemia, or is it because you're not reabsorbing the sodium in the thick ascending limb, which leads to increased Na+/K+ exchange in the collecting duct?

 

[PMPMD]

Why does furosemide often cause hypokalemia?

My understanding is that it inhibits the NKCC2 co-transporter in the thick ascending limb of the loop of Henle, so is it the reduced K+ reabsorption here that leads to the hypokalemia, or is it because you're not reabsorbing the sodium in the thick ascending limb, which leads to increased Na+/K+ exchange in the collecting duct?

Both.

 

[LouisianaDoctor]

1. I will limit my answer to acute kidney injury (AKI), as I'm a critical care fellow and that's where most of my experience lies. The evidence regarding the use of loop diuretics in AKI is inconsistent. The bulk of the evidence shows there is no effect either way on the course of AKI with loop diuretics. Again, in the specific case of AKI, we administer diuretics not to alter the course of AKI but rather to manage the extra-renal complications, for example, pulmonary edema.

Thank you kindly for answering.

So what do we make of rising BUN/Cr in patients on Lasix? Is the Lasix causing the rise?

 

[PMPMD]

Thank you kindly for answering.

So what do we make of rising BUN/Cr in patients on Lasix? Is the Lasix causing the rise?

Depends. If the pt's prerenal then it might be. If the cause is intrinsic renal, it could just be the underlying course.

 

[Instatewaiter]

Hi all,

1. One thing I don't understand is how we should interpret BUN/Cr in these patients. For example, if I'm giving a patient Lasix and their BUN and Cr are rising, what is this telling me? Is this Lasix damaging the kidneys, or is it telling me that I am removing fluids from the patient and things are "concentrating" (ie, the same concentration of BUN, but in a smaller volume.) Is this when I should look for a > 20:1 BUN/Cr ratio?

2. When administering IV Lasix, when do you make the switch back to PO? I've been told that you can switch back to PO if the patient is symptomatically improving, or if they experience a bump in their Cr. And how would you convert the dose back to PO? Would you have to double it?

3. What is the difference between giving someone, for example, 80 mg of Lasix IV BID, as opposed to a 20 mg/hr drip? I understand the quantity given will be different, of course, but why would I pick a drip?

Thank you kindly for any insight.

1) Screw the BUN/Cr ratio. It is sometimes helpful, often times not. As your intravascular volume is depleted, you should see the BUN rise. This doesn't mean they are getting euvolemic or dry. As you start removing intravascular volume the BUN and HCO3 are going to rise and they still may be overall volume overloaded .

It is often hard to tell if there is "kidney damage" or just less volume. Frequently you will see the BUN and Cr rise and the patient will still have lots of extravascular volume (ie still overall volume up). You often have to let the extravascular volume and intravascular volume equilabrate (pause diuresis) and then start the diuresis after they move some of that extravascular volume back into their vascular space. It is useful to look at the Na (is it changing) and the HCO3 (is it going up) to tell if you are getting close to intravascular euvolemia.

2) Because of extensive gut edema, PO lasix sucks if someone is really volume overloaded. Torsemide and Bumex are much better but still not ideal. If they are in the hospital they should be on IV lasix unless the volume is not their main issue. If they are gettting close to euvolemic (ie based on JVP that is just slightly elevated) you can switch them back to PO and discharge them.

3) IV lasix vs a drip- there are a few times to pick a drip:
a) you are worried about the vasodilatory effects of lasix on blood pressure (ie they are dropping their pressure to your lasix slugs). The drip is a lot more gentle and gives a continuous effect on preload. This is especially impt for preload dependent conditions (R sided MI, constriction, Aortic stenosis etc).

b) When you are having difficulty diuresing. Sometimes people just diurese better on a drip. With slugs of lasix, you often get very salt avid between doses. This sometimes works against you when you are trying to diurese. A drip prevents this salt avid state because you are continuously exposing the kidney to a loop diuretic.

c) Your attending tells you to put them on a drip

 

[LouisianaDoctor]

1) Screw the BUN/Cr ratio. It is sometimes helpful, often times not. As your intravascular volume is depleted, you should see the BUN rise. This doesn't mean they are getting euvolemic or dry. As you start removing intravascular volume the BUN and HCO3 are going to rise and they still may be overall volume overloaded .

It is often hard to tell if there is "kidney damage" or just less volume. Frequently you will see the BUN and Cr rise and the patient will still have lots of extravascular volume (ie still overall volume up). You often have to let the extravascular volume and intravascular volume equilabrate (pause diuresis) and then start the diuresis after they move some of that extravascular volume back into their vascular space. It is useful to look at the Na (is it changing) and the HCO3 (is it going up) to tell if you are getting close to intravascular euvolemia.

2) Because of extensive gut edema, PO lasix sucks if someone is really volume overloaded. Torsemide and Bumex are much better but still not ideal. If they are in the hospital they should be on IV lasix unless the volume is not their main issue. If they are gettting close to euvolemic (ie based on JVP that is just slightly elevated) you can switch them back to PO and discharge them.

3) IV lasix vs a drip- there are a few times to pick a drip:
a) you are worried about the vasodilatory effects of lasix on blood pressure (ie they are dropping their pressure to your lasix slugs). The drip is a lot more gentle and gives a continuous effect on preload. This is especially impt for preload dependent conditions (R sided MI, constriction, Aortic stenosis etc).

b) When you are having difficulty diuresing. Sometimes people just diurese better on a drip. With slugs of lasix, you often get very salt avid between doses. This sometimes works against you when you are trying to diurese. A drip prevents this salt avid state because you are continuously exposing the kidney to a loop diuretic.

c) Your attending tells you to put them on a drip

I just wanted to thank you for this post. It really made sense and helped me understand what is going on.

 

[dienekes88]

Maybe wiser heads will disagree with me. Perhaps they already have?

Hi all,

I have a few questions regarding Lasix. I understand the indications and how it works. I know that IV Lasix is twice as "potent" as PO Lasix, and I know several ways to figure out a initial dose of Lasix in the inpatient setting. However, I have many questions about its use in this setting.

1. One thing I don't understand is how we should interpret BUN/Cr in these patients. For example, if I'm giving a patient Lasix and their BUN and Cr are rising, what is this telling me? Is this Lasix damaging the kidneys, or is it telling me that I am removing fluids from the patient and things are "concentrating" (ie, the same concentration of BUN, but in a smaller volume.) Is this when I should look for a > 20:1 BUN/Cr ratio?

I learned it a different way. If you are arterially underfilled, then there is a non-osmotic impetus for ADH secretion. When you are diuresing someone, they release ADH, because there is the perception that the body is arterially underfilled. After all, the kidneys wanted to hold onto that volume for a reason in the first place, right? An increase in the BUN/Cr ratio is simply a sign that the body senses this arterial underfilling and is releasing ADH to recapture water. Urea is freely mobile, so it will move with that water.

This is the same mechanism by which heart failure patients get hyponatremic.

If you see a creatinine bump, then your patient may be pre-renal.

The best way to monitor your diuresis is to follow the weight. You should know your patient's dry weight.

Why does furosemide often cause hypokalemia?

My understanding is that it inhibits the NKCC2 co-transporter in the thick ascending limb of the loop of Henle, so is it the reduced K+ reabsorption here that leads to the hypokalemia, or is it because you're not reabsorbing the sodium in the thick ascending limb, which leads to increased Na+/K+ exchange in the collecting duct?

Again. My understanding is different.

The decrease in volume leads to a baroreceptor mediated increase in renin secretion from the juxtaglomerular apparatus. This leads to an increase in the conversion of Angiotensinogen to Angiotensin I followed by conversion to Angiotensin II. Angiotensin II then stimulates the zona glomerulosa of the adrenal cortex to secrete aldosterone.

Here's where we get back to the tubule. There is increased delivery of sodium to the distal tubul with Lasix, and Aldosterone mediates the placement of ENaC channels to reabsorb that sodium. Protons and potassium move out to balance the ions.

This mechanism also explains the phenomenon of paradoxic aciduria in a patient with pyloric stenosis.

1) Screw the BUN/Cr ratio. It is sometimes helpful, often times not. As your intravascular volume is depleted, you should see the BUN rise. This doesn't mean they are getting euvolemic or dry. As you start removing intravascular volume the BUN and HCO3 are going to rise and they still may be overall volume overloaded .

I didn't learn it as volume status. I learned it as the state of being arterially underfilled, but my explanation easily fits within the fold of yours.

 

[CaptainSSO]

Again. My understanding is different.

The decrease in volume leads to a baroreceptor mediated increase in renin secretion from the juxtaglomerular apparatus. This leads to an increase in the conversion of Angiotensinogen to Angiotensin I followed by conversion to Angiotensin II. Angiotensin II then stimulates the zona glomerulosa of the adrenal cortex to secrete aldosterone.

Here's where we get back to the tubule. There is increased delivery of sodium to the distal tubul with Lasix, and Aldosterone mediates the placement of ENaC channels to reabsorb that sodium. Protons and potassium move out to balance the ions.

This mechanism also explains the phenomenon of paradoxic aciduria in a patient with pyloric stenosis.

Thanks. I was intuitively feeling like aldosterone should be involved in the hypokalemia but I wasn't connecting the dot.

So for pyloric stenosis, you're saying pyloric stenosis ---> projectile vomiting ---> loss of extracellular fluid and H+ ----> alkalosis + low ECF volume ---> low ECF activates RAA system ----> increased Na+/H+ exchange at CCD, urinary acidosis?

 

[dienekes88]

Thanks. I was intuitively feeling like aldosterone should be involved in the hypokalemia but I wasn't connecting the dot.

So for pyloric stenosis, you're saying pyloric stenosis ---> projectile vomiting ---> loss of extracellular fluid and H+ ----> alkalosis + low ECF volume ---> low ECF activates RAA system ----> increased Na+/H+ exchange at CCD, urinary acidosis?

Yes.

You also have to remember that in someone who is volume down there will be a non-osmotic impetus for ADH secretion. For this reason, the patient will likely also be hyponatremic. Sodium concentration is a reflection of water metabolism and not salt handling.