Hyperkalemia is bananas

Two cases of hyperkalemia in Red clinic this week uncovered a weakness in my own understanding of this issue.  What to do?  Write a blog post, of course.

Potassium balance occurs by moving potassium in and out of cells (thanks to all those pumps that you learned about in medical school) and regulating renal excretion of potassium (more pumps).

Hyperkalemia is due to either too much potassium released from cells or not enough potassium excreted by the kidney.

Cells first
  • Acidosis causes potassium to leave the intracellular space as H+ ions enter
  • Hyperglycemia (DKA), it’s not so much the acidosis in this instance as it is the loss of intracelluar K due to osmotic forces from the hyperglycemia
  • Tissue breakdown- seen most often in tumor lysis syndrome or trauma
To the kidneys
  • Reduced aldosterone secretion: with nl underlying renal function, this is usually a small rise in K.
    • Hyporeninemic hypoaldosteronism
      • RX: NSAIDS, Calcineurin Inhibitors
      • Acute glomerulonephritis
      • Renal insufficiency- most common with diabetic nephropathy
    • RX: Angiotensin system blockers (leads to rise in renin levels)
    • RX: Heparin (usually chronic therapy) can be directly toxic to zona glomerulosa cells
    • Adrenal Insufficiency (only primary AI, the pituitary is not a big regulator of aldosterone)
    • Inherited disorders (that I am conveniently ignoring here)
  • Reduced response to aldosterone
    • RX: Potassium sparing diuretics (spironolactone), trimethoprim (1/2 of Bactrim)
    • Pseudohypoaldosteronism Type 1 (another, albeit well named, congenital disorder that I am ignoring for now)
  • Reduced distal sodium/water delivery (turns off the pumps): anything that decreases effective circulation volume, meaning that dehydration/hypovolemia AND hypervolemia in CHF or cirrhosis can be blamed.
    • Key scenario here is the decompensated CHF patient with poor renal perfusion as they fall off the Starling curve, yet continue their ACE inhibitor and Aldactone.
  • Acute or chronic kidney disease: typically it takes some renal hit (new or ongoing) plus one of the other things above to get truly clinically significant hyperkalemia.  Key scenarios:
    • The fasting dialysis patient.  They are missing the insulin which helps maintain the potassium balance.  This is why we give insulin and glucose  IV when we keep ESRD patients NPO in the hospital.
    • Late stage CKD patients who eat a high potassium diet.  Most patients can eat all the bananas they want and not get hyperkalemia.  Not so if your GFR is 20.
  • Ureterojejunostomy (neobladder). The jejunum (that was used to make the bladder) absorbed potassium in a former life.  Still does.
So how to make the diagnosis?
Think about the etiologies listed above.  What fits for your patient? Look closely at medicines and renal function.
Is this an out of the blue hyperkalemia?  Maybe it’s pseudohypokalemia/lab error- recheck.
If it is an acute rise (that you are pretty sure is real), think moving potassium out of cells.  Tumor lysis syndrome?  DKA?  Acidosis?
If you are still stuck, look to the kidneys. Figure out if aldosterone is working correctly.
  • Check Plasma Renin Activity (PRA), Plasma Aldosterone, and Plasma Cortisol.  Ideally checked after patient is upright for 3 hours (not the time for the 8am cortisol value), or after being given a dose of lasix.
    • Hyporeninemic Hypoaldosteronism- Type 4 RTA will have Low PRA, Low Aldosterone, normal cortisol
      • Usually 50-70 yo diabetic patients with mild/moderate renal insufficiency
    • Primary AI: low aldosterone, low cortisol. Nl or high PRA

Diabetes Education

First, welcome to new readers!  I’ve kept this blog kind of quiet for the last few months, but feedback has been good, so I am rolling it out to the whole residency today.  Lucky you!

You can sign up for email updates to the right
follow me on twitter @ihaterashes
like the University of Alabama at Birmingham, Division of General Internal Medicine Facebook Page  

(look at me, all social media literate and stuff, so cute)

Just a quick post today about diabetes education as it came up in IM IV clinic last week.  Both VA and UAB have great help available to you for teaching your patients about their diabetes.  It is a life changing diagnosis and really hard to adequately cover in an office visit, even if you didn’t also have to talk about hypertension and back pain and obesity and cancer screening and…

At TKC- you can choose: Diabetes education, AMB (hint, save it as a favorite)
at VA, it is under consults: Diabetes Nurse, Patient Ed.

Services at both places include dietary education, glucometer teaching, insulin administration (including basal/bolus regimens), counting carbs, what do to on sick days, and recognizing and managing hypoglycemia.  They also cover things like eye and foot health, long term complications, and managing stress.

Medicare and BCBS pays for 10 hours of education once (ideally after diagnosis, but ok to refer someone diagnosed 20 years ago, if they never got any teaching), then 2 hours every year after that. At UAB, the first course is 5 hours, then there is a 2 hour follow up course.  The refresher course is 2 hours.  The diabetic educators will send you the pre/post tests of your patients, and you can highlight the things that tripped them up on the test.

At the VA, there is both a comprehesive diabetes managment group class and 1:1 education for insulin administration and complications managment. 

There is also a great website developed by the Division of Preventative Medicine here at UAB with a lot of (mostly free) resources for diet, exercise and medication managment. 

Sadly, none of the payers are covering nutrition education for non-diabetics (or pre-diabetics) quite yet. You can get nutrition education for your patients at the VA with the MOVE 123 program.   Hopefully now that obesity is a “disease”, we’ll start to see more reimbursment.  In the  meantime, here’s something we can all agree on.