Responding to Hyperkalemia

Last week, we discussed the rationale for how we respond to calls about hyperkalemia.  Coincidentally, a new article came out on this topic in the CMAJ.

The essential points in our discussion were:

1.  Make sure it's real - order repeat bloodwork to ensure you don't respond inappropriately to hemolyzed blood samples, mislabelled samples, or problems with blood collection technique that give rise to spuriously high K+ in the tube, but not in the patient.

2.  Assume that it is real until you know otherwise - while waiting on the above, don't hesitate to respond to the K+ value that you do have, especially if it is greater than 6.0, or the clinical setting is likely to promote hyperkalemia (see below).

3.  Assess the consequences of the hyperkalemia.  The most frequently cited thing to do next is to "look for ECG changes".  While this isn't wrong, don't be misled by their absence - a recent review found them to be very infrequent!  The ECG changes are:

• Tall, "tented" or "peaked" T waves
• Loss of P waves
• Shortening of PR interval
• Widening of QRS
• Loss of SA node activity and evolution of a "Sine Wave"
• Asystole

Perhaps more importantly, check for hemodynamic consequences.  Rising K+ levels don't just affect conduction - they also affect contractility, and falling BP may be a result of this.

4.  Assess the setting for possible causes.  This isn't just a follow-up step - start thinking of this RIGHT AWAY.  Your immediate management may be guided by this.  The approach to diagnosing the cause looks for each of:

• high intake (almost always in combination with reduced clearance, and almost always involving a physician administering potassium somehow);
• reduced clearance - renal compromise (lowered GFR) is by far and away the most common association with hyperK.  Look out for meds that also affect renal K handling, eg. spironolactone.
• shift -  the big player here is acidosis, which you need to identify early in order to help the K.

Special mention:  ALWAYS ascertain whether the patient is on Digoxin.  Hyperkalemia related to digoxin toxicity requires specific management! (Get the full article from U of T here.)

5.  Start Managing the K+!

• Get help.  Trying to manage patients on your own, especially when they have potassium levels >6.5, can set them up for disaster if things get out of control quickly. Get the crash cart if there are ECG changes or the patient is symptomatic, or if the K level is >7.0.  At a minimum have a nurse nearby to handle all the IV access issues and assist monitoring the patient.
• Protect the heart.  Give Calcium salts (CaCl2 or Ca gluconate), usually as a rapid infusion over 2-10 minutes.  In pre-arrest situations, you may need to give by direct injection over about 30 sec.  (Always have ECG monitoring in place for this.)  NB.  This does nothing for the K level.  It only buys you time.  However, it can have some dramatic clinical effects - I have personally raised someone's BP from 60 to 90 systolic with Ca gluconate alone.
• This is one of the differences with digoxin toxicity - DON'T give Ca salts to these patients!
• Start shifting the potassium.  You can give nebulized ventolin as a start.  10 units of REGULAR insulin followed by 50 mL of 50% dextrose will also bring the K+ down somewhat. 
• If the patient is extremely acidotic, and not volume overloaded, you should consider infusing sodium bicarbonate to assist in shifting the potassium back into cells.  This is NOT part of the routine management of this problem - only done in specific situations!
• Start eliminating the potassium.  All the shifting in the world won't solve the problem, unless the total body K+ has been brought down to normal.  
• If the patient makes any urine at all, it's worth trying to assist K excretion via the kidneys, using loop diuretics.  This can be the most efficient route of K excretion.
• Otherwise go for the GI route to excrete K.  Use K-binding resins (prefer calcium resonium for volume overloaded patients, rather than sodium polystyrene, because it avoids loading them with sodium).  Remember that resins without sorbitol cause a lot of abdominal pain, and not much K excretion - give them plenty of sorbitol to help things move along osmotically.

6.  All of this may not be enough.  Patients with very little renal function may only get their potassium down reliably with dialysis.  If you are seeing a patient with newly diagnosed renal failure, treat as above, and get help from a nephrologist to assess whether dialysis should be instituted on an emergency basis.