Hyperkalemia April 14th 2015

Hyperkalemia

Potassium is often found mostly  intracellular, majority of it is reabsorbed, about 10% of our potassium losses is through our GI tract. The reason we talk about high potassium is that it can kill us via cardiac arrhythmia, low potassium can do the same so we need it just right!

There are no specific symptoms of high potassium – fatigue, weakness, decrease reflexes (but one of our approach to fatigue is checking lytes to look for high potassium).

To be honest, I’ve yet to find a nice and neat all encompassing approach to hyperkalemia.

However my approach is as follows:

Firstly make sure its real! (hemolysis of the sample: often with PICC lines, clenched fists, can be seen in CLL with high lymphocytes!)

** tip: if you REALLY need to know you can do lytes via ABG, comes back quick and accurate, this also helps you distinguish pseuduohyponatremia in the setting of multiple myeloma.

***tip: If you really uncertain whether the potassium of 7 is real, you could do a stat ECG

Decreased secretion: in the setting of decreased perfusion to the kidneys, also less sodium delivery prevents potassium secretion because of a N+/K+ exchange in the distal convoluted tubule. Remember angiotensin II gets unregulated in dehydration, it works on the cortex of the kidney to excrete aldosterone, hence why ACEI can effect potassium. ALWAYS check creatinine when checking potassium as it gives context (AKI?).

 Anything that effects aldosterone which also gets rid of H+ and K+ can cause potassium to increase – addisons, ACEI/ARBS/ spironolactone which will effect potassium secretion. Septra inhibits secretion at DCT and needs to be considered when putting patients on potassium sparring diuretics.

Type IV RTA is a rare cause of hyperkalemia  and is most commonly seen in diabetics, aldosterone is not as effective on the DCT.

Increased body production: This is where scary things like tumor lysis syndrome, Rhabdo, and intravascular hemolysis need to be considered.

Shift out of cells:  acidosis and lack of insulin are the two big things! Acidosis is because the blood wants to balance pH above everything, when there is an increased amount of H+ (acidosis) from sepsis, a loss of bicarb with diarrhea, etc. H+ will be buffered out of the vasculature to try and balance pH. As the H+ moves out, K+ moves intravascular to balance the charge. HENCE Acidosis = Hyperkalemia. Insulin shifts potassium inside cells as well as glucose so a lack of it will cause hyperkalemia… and if you remember, when treating DKA we GIVE potassium when the patient’s labs are high normal 5.2 because we know it will drop with insulin therapy.

*More obscure causes – beta blockers (makes sense because we USE beta agonists to shift high potassium), and heparin is also associated with high potassium in hospital.

Increased production: Rare, but maybe patients with renal impairment were just left on IV potassium replacement or there are certain foods (noni juice>) etc. may contain high amounts, also some patients maybe taking high amounts of potassium supplementation for alternative medical therapy.

ECG findings is peaked T waves, and potentially heart block or wide QRS. That’s why we always check lytes in the setting of heart block!

Treatment is outlines in the

1.      Most sources will use potassium >6.5 as severe, if you believe it to be true or ECG shows peaked T waves, give calcium gluconate 1 gram (1 amp) IV to protect the heart. Caution with dig toxicity.

2.      Shift with 1 amp of D50 (25-50 g of glucose), followed by 10 units of regular insulin IV which will last around 2-6 hours.

3.      Consider beta agonist salbutamol with 10-20 mg nebs

4.      Ensure urine output! Foley catheter, Normal saline, can give IV boluses of 500. Be aware of resp function, are they in AKI and building up fluid?

5.      Kayexlate 30 g followed by lactulose 30 mL po. Need a bowel movement! Has been associated with necrosis bowel so avoid in ileus, post op, or patients on heavy doses of narcotics.

6.      Sodium Bicarb – in patients with CKD, this functions two fold. By making an alkalotic environment, it shifts potassium into cells, and by increasing sodium delivery to distal nephron, it will activate the N/K+ exchanger to kick out more potassium.

7.      Nephrology consult? If patient not urinating, or unable to shift potassium, or the patient is severely overloaded and worried about giving fluids to pee it out, dialysis may be the best option.

Be aware that all this shifting is fine and dandy but if they can’t urinate you have yourselves a problem! If they can urinate, giving them lots of fluids may be the best thing… if they get overload, Lasix can be given which will ALSO lower potassium.