Hyperkalemia Call Review

[E tank]

Just wanted to make a quick couple points...



Absolutely. Insulin, usually given with dextrose, does cause intracellular shift of potassium. And in a pinch, both are generally readily available in most patient care areas.

Practically, however, I have found insulin:d50 therapy to be very unpredictable, both in its efficacy and the duration of the effect. This seems to hold especially true in acidotic patients, who oftentimes laugh at insulin.

That being said, I give it anyway. And most of the ER docs do as well, I have found.

Just to put a little perspective on this entire conversation, you guys bring us incredibly hyperkalemic dialysis patients all the time. You just aren't around when the labs result. That patient that missed a dialysis run or two, it's nothing for his K to be 7+. The septic ESRD patient, also frequently 7+. As these patients go through years of potassium buildup and washout on dialysis, they adapt. They tolerate higher potassiums in stride. We treat them anyway, but truth be told most would likely be fine until dialsysis can get started.

Honestly, what most hyperkalemic emergencies really need is fluids. In my experience, volume expansion has been far and away the most effective method of quickly lowering plasma potassium concentration. Recall that the potassium "level" is actually a measure of concentration, dissolved in plasma and measured in meq/L. Humans have 40ml of plasma per kg of body weight. So in a 75 kg patient, about 3L of total plasma volume. Mathematically, you can imagine how effective adding a liter or two to that would be in decreasing the plasma concentration.

Fluids open, gram or two of calcium. Bicarb if they have a metabolic acidosis. Gentle hyperventilation if they don't. Loop diuretics if the kidneys work. Dialysis or CRRT if they don't.

The insulin-dextrose is usually an afterthought for me. Laxatives are only for revenge. Albuterol, sure why not. But they aren't terribly effective, honestly.

You have the best treatment readily available for $0.19/L.

I think you nailed it when you referenced the acidemic patient not responding to the insulin/dextrose cocktail. They don't respond to much of anything in the way of ino/pressor support either until that is fixed to one degree or another. In the highly artificial world of the OR, insulin/dextrose works very effectively and predictably, but that is when there is no acidemia, and the patient is normothermic and euvolemic. Even adding bicarb to someone that is not acidemic works pretty well with hyperkalemia when they are "perfectly" tuned. Not reality in emergency/CC, I know.

But I wonder how volume overload changes your strategy in these patients that have missed a couple of days of dialysis?

 

[VentMonkey]

Not reality in emergency/CC, I know. But I wonder how volume overload changes your strategy in these patients that have missed a couple of days of dialysis?

In the emergent prehospital setting, not a whole lot one can do. 9 times out of 10 these patients present as the classic "flash pulmonary edema" with chief complaints of chest discomfort, and/ or dyspnea.

A well versed prehospital clinician should be able to put the pieces together for the receiving ED staff in order to hopefully push the patient towards the emergency dialysis route. Aside from the likelihood of th said patient getting CPAP in the field for flash edema, performing 12 leads, perhaps placing the patient on pads, and/ or monitoring for acute and lethal arrhythmias (i.e., sine waves) there isn't much else that would change their outcome in the field.

Sure, the aforementioned cocktail everyone has eluded to will buy the time, but that's all it will do. For me less is more in an urban setting with reasonably short transport times. Perhaps and order for CaCl- PRN from the base in line with the "hey, 'X' patient needs emergency dialysis" in the face of extended transport times.

As far as the CCT setting, more often than not the sending is way ahead of the curve regarding the cocktail, but if not, I doubt it would be hard to argue against any standing orders/ consults with the sending, receiving, or both physicians. In the event that the patient required emergency intubation en route to the receiving facility, I would be more concerned with knowing the patients most recent lab work, as well as medical history and co-morbidities to properly reflect their ventilator settings.

This is alljus my spin on an out-of-hospital management style. Merely one way to skin the proverbial cat...

 

[StCEMT]

What are y'all a thoughts on furosemide in these folks? I have it available, but I have no first hand experience with it. Also, in the event of pulmonary edema, would you still make an effort to give fluids after trying to help the edema? Or just let it be and the hospital can deal with it (time allowing).

 

[VentMonkey]

What are y'all a thoughts on furosemide in these folks? I have it available, but I have no first hand experience with it.

Lasix has fallen out of favor in the prehospital setting given is likelihood to increase ICU stays. Most of these patients are RF/ ESRD patients, and oftentimes are on more Lasix than I could ever double up on.

Nowadays when I think Lasix, it's more along the lines of a DI, or SIAD patient. Neither of which, I would be treating aside from supportive care in the field.

Also, in the event of pulmonary edema, would you still make an effort to give fluids after trying to help the edema? Or just let it be and the hospital can deal with it (time allowing).

St, this is where the term "judicious fluid bolus" has a definite place. Frequent reassessments for worsening fluid shifts, third spacing, JVD, adventitious breath sounds, etc. are--as you're aware--crucial.

Walking that fine line of a "PAP-able" patient as well as one who needs fluid isn't worth withholding volume resuscitation if they need it, again, so long as it's prudently judicious.

 

[NPO]

Just wanted to make a quick couple points...



Absolutely. Insulin, usually given with dextrose, does cause intracellular shift of potassium. And in a pinch, both are generally readily available in most patient care areas.

Practically, however, I have found insulin:d50 therapy to be very unpredictable, both in its efficacy and the duration of the effect. This seems to hold especially true in acidotic patients, who oftentimes laugh at insulin.

That being said, I give it anyway. And most of the ER docs do as well, I have found.

Just to put a little perspective on this entire conversation, you guys bring us incredibly hyperkalemic dialysis patients all the time. You just aren't around when the labs result. That patient that missed a dialysis run or two, it's nothing for his K to be 7+. The septic ESRD patient, also frequently 7+. As these patients go through years of potassium buildup and washout on dialysis, they adapt. They tolerate higher potassiums in stride. We treat them anyway, but truth be told most would likely be fine until dialsysis can get started.

Honestly, what most hyperkalemic emergencies really need is fluids. In my experience, volume expansion has been far and away the most effective method of quickly lowering plasma potassium concentration. Recall that the potassium "level" is actually a measure of concentration, dissolved in plasma and measured in meq/L. Humans have 40ml of plasma per kg of body weight. So in a 75 kg patient, about 3L of total plasma volume. Mathematically, you can imagine how effective adding a liter or two to that would be in decreasing the plasma concentration.

Fluids open, gram or two of calcium. Bicarb if they have a metabolic acidosis. Gentle hyperventilation if they don't. Loop diuretics if the kidneys work. Dialysis or CRRT if they don't.

The insulin-dextrose is usually an afterthought for me. Laxatives are only for revenge. Albuterol, sure why not. But they aren't terribly effective, honestly.

You have the best treatment readily available for $0.19/L.

Thank you for your insightful comments!

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