Master the management of hyperkalemia with tools, tips and tactics from @kidney_boy, Joel Topf MD, Chief of Nephrology @KashlakHospital. We cover: common causes of hyperkalemia; the U-shaped curve of potassium levels and mortality; albuterol nebs; how to safely use insulin; potassium binding resins and colonic necrosis; Does it make sense to give loop diuretics and fluids?; Should we be using fludrocortisone?; Plus, answers to all your questions about a high potassium diet and oral potassium supplements! Join us for Dr Topf’s masterful insights on hyperkalemia and potassium homeostasis. Get deeper into potassium physiology with a FREE pdf copy of Joel’s book The Fluid Electrolyte and Acid Base Companion here.
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Written and produced by: Matthew Watto, MD
Hosts: Matthew Watto MD, Paul Williams MD, Stuart Brigham MD
Infographic: Matthew Watto MD
Edited by: Matthew Watto MD
Guest: Dr Joel Topf MD
“If you can treat your medical student like a pneumatic tube then you can get a clean potassium measurement.”-Dr Topf jokingly teaches us how to avoid pneumatic tube related pseudohyperkalemia.
Hyperkalemia is usually caused by one of three mechanisms: Increased potassium intake [e.g. food, enteral feeds, TPN, meds (PCN), IV fluids, dialysate, PRBCs], Transcellular potassium shifts (e.g. rhabdomyolysis), or Impaired potassium excretion (e.g. AKI, CKD, aldosterone antagonism, RAAS inhibition). Joel notes that chronic hyperkalemia is almost always from impaired excretion.
Pseudohyperkalemia is common. Ask yourself, “Does it make sense for this patient to have hyperkalemia?” If not, then look for causes of pseudohyperkalemia (e.g. very high WBC or platelet count, difficult phlebotomy, pneumatic tube induced trauma)
EKG changes are NOT sensitive for hyperkalemia and could miss up to 39% of patients even with a K+ of 7 to 9 mEq/L. Under 50% who developed dangerous arrhythmias or death had EKG changes [Montague Clin J Am Soc Neph 2008 – PMID18235147].
The sweet spot for potassium appears to be a mean K+ of 3.5 to 4.5 mEq/L [Goyal JAMA 2012 – PMID22235086]. There is not a well defined treatment threshold.
Rule out acute urinary obstruction and hyperglycemia in patients with acute hyperkalemia. –Dr Topf’s expert recommendationDr Topf recommends using the kidneys to excrete excess potassium as a first line option. Employ some combination of loop diuretics, saline, and/or fludrocortisone.
Hypoglycemia is common (~13%) when using IV insulin to treat hyperkalemia. Joel recommends monitoring glucose every 30 minutes for 4-6 hours afterwards.
SPS (sodium polystyrene sulfonate) is effective for potassium excretion via the GI tract. Dr Topf recommends use in patients who cannot increase urinary excretion. Caution: Intestinal (colonic) necrosis is a rare complication. BUT, Joel avoids SPS in patients with a “sick bowel” or recent kidney transplantation.
Dietary potassium is usually in the form of potassium phosphate, which increases urinary excretion of potassium. For this reason, increasing dietary potassium is a poor option for HYPOKALEMIA. Joel notes potassium supplements may lower blood pressure. Additionally, hypokalemic patients in ALL-HAT had increased mortality. Therefore, monitor for hypokalemia and supplement using potassium chloride (or Morton’s LITE salt)!
The distal nephron (distal convoluted tubule aka DCT) contains the ENac channel. This epithelial sodium (Na+) channel reabsorbs Na+ into the tubular cells leaving a net negative charge in the lumen. Consequently, potassium leaves the cells (attracted to the negatively charged tubular lumen) and is excreted in the urine. This mechanism can be exploited to treat hyperkalemia [see figure below from Joel’s book or just get the pdf here].
Therapeutic example: IV saline and/or loop diuretics → increased distal sodium delivery → sodium passes into tubular cells via the ENac channel → tubular lumen develops net negative charge → potassium leaves cells for lumen → potassium is excreted in the urine.
Acute hyperkalemia can involve all three mechanisms. But, chronic hyperkalemia is usually due to impaired excretion. Thus, it’s best to optimize potassium excretion in chronic hyperkalemia. Potential strategies include: lower dose or limit use of ACEI (and ARBs), add a diuretic, and/or neutralize metabolic acidosis with oral bicarbonate
About 98-99% of total body potassium is located inside the cells. It doesn’t take much cell damage to raise the serum potassium. -Dr Topf explaining why pseudohyperkalemia is so common.
Common causes of pseudohyperkalemia include: A very high WBC count (e.g. leukemia) or platelet count (above one million); phlebotomy (either difficult stick or poor blood flow into the syringe); vigorous fist pumping; and trauma from the pneumatic tube system.
Kashlak pearl: Ask yourself, “Does it make sense for this patient to have hyperkalemia?”. If not, then consider pseudohyperkalemia.
An EKG has poor SENSITIVITY for hyperkalemia (SPECIFICITY is probably “decent”). One study, found T wave abnormalities were present in only 39 percent of patients with potassium of 7 to 9 mEq/L. The 14 patients with damaging arrhythmias or cardiac arrest only had EKG changes about 50 percent of the time [Montague Clin J Am Soc Neph 2008 – PMID18235147]. A study of dialysis patients found no relationship between T wave amplitude and hyperkalemia [Aslam Nephro Dial Transp 2002 – PMID12198216].
Lisa Einhorn et al conducted a study on when to treat hyperkalemia. It looked at death within 24 hours in relation to potassium level. The odds ratio for death was 10 at a potassium of 5.5 to 6 mEq/L. It rose to 31 for potassium above 6! [Einhorn Arch Int Med 2009 – PMID19546417] NOTE: There is a not a well defined treatment threshold. This algorithm from the NHS suggests acute therapies and monitoring if K+ >6 mEq/L with EKG changes or >6.5 mEq/L regardless of EKG [NHS guidelines Oct 2018].
Actually, there is a U-shaped curve. The safe potassium range seems be 3.5 to 4.5 mEq/L. —A JAMA study from 2012 looked at the mean serum potassium for patients with admitted with acute myocardial infarction. It found that mortality was highest outside the range of 3.5 to 4.5 mEq/L [Goyal JAMA 2012 – PMID22235086].
Kashlak pearl: The first choice in hyperkalemia is to get rid of potassium in the urine. Dr Topf mainly uses SPS or other potassium binding agents in patients who are anuric.
Dr Topf reminds us to rule out acute urinary obstruction because it causes a “specific potassium secretion defect in the kidney.” Consider a bladder scan.
Check blood glucose because hyperglycemia causes “solute drag”. Intracellular fluid leaves the cell and drags potassium with it. Additionally, a relative lack of insulin promotes hyperkalemia by impaired potassium uptake.
Loop diuretics block proximal sodium absorption. Thus, they increase distal sodium delivery and reabsorption through the ENac channel. Similarly, an IV saline infusion directly increases distal sodium delivery/absorption. Dr Topf notes, combination therapy with a loop diuretic and saline can be used for hyperkalemia, hyponatremia and hypercalcemia in certain treatment protocols.
Fludrocortisone 0.1 or 0.2 mg twice daily will lower potassium over 1 to 2 days. Downsides include: hypertension and sodium retention. Thus, use caution in patients with congestive heart failure. The ideal patient is one with hyperkalemia from chronic hyporeninemia and hypoaldosteronism (e.g. patients with diabetes and Type 4 RTA). Successful therapy was also reported in case series of kidney transplant recipients with refractory hyperkalemia.
Administer dose of 10 to 20 mg. This is eight nebulizer treatments back to back! Needless to say, patients will feel jittery and develop tachycardia. That said, Dr Topf notes this is generally safe. Additionally, there is data to suggest that patients on beta agonists get less hypoglycemia! [Saleh Diabetes Care 1997 – PMID9250445 ; Phillipson J Allerg Clin Immunol 2002 – PMID12464941]
IV insulin drives potassium into the cells. It should be given with IV glucose to prevent hypoglycemia. Dr Topf notes, consider omitting the glucose if a patient already has hyperglycemia.
Kashlak pearl: The incidence of hypoglycemia approaches 13 percent [Apel Clin Kidney J 2014 – PMC4377748 ]. The kidney metabolizes insulin and also performs gluconeogenesis. Thus, patients with CKD are at high risk for hypoglycemia. Joel checks the glucose every 30 minutes for 4 to 6 hours.
Each vial of calcium chloride has three times the calcium load of calcium gluconate. Thus, it has more effect when treating EKG changes from hyperkalemia. Guidelines recommend giving calcium for EKG changes. The effect is instant, but is not long lasting. Therefore, repeat doses are often necessary. Repeat the dosing (usually max of 3 doses) until the EKG normalizes [NHS guidelines Oct 2018].
It was grandfathered into use by the FDA after two 1961 NEJM studies, which were “garbage” by modern standards. In 2015, an RCT of patients with CKD 4-5 and hyperkalemia found daily SPS lowered potassium [Lepage Clin J Am Soc Neph 2015 – PMID26576619]. Actually, some patient developed hypokalemia!
SPS was reported to cause colonic necrosis in an initial case series [Gerstman AJKD 1992]. Subsequently, a systematic review found 58 cases in the literature [Harel Am J Med 2013 – PMID23321430]. In 1991, a letter to Am J Kidney Disease estimated 35,000 kg (or 1.5 million doses) of SPS are used each year. Thus, 37 million doses were used in a 25 year period with only 58 reported cases of colonic necrosis. Even if the number of cases is 1000 times higher than reported, then the incidence is still only about 0.15 percent (Joel’s back of the envelope calculation). Therefore, it seems to be a rare complication. “Clinically, we just don’t see it that often” notes Dr Topf.
Kashlak pearl: Dr Topf avoids SPS in patients with renal transplant or a “sick bowel” e.g. recent surgery, bowel obstruction, GI bleed, etc. Consider SPS or other binding agents in patients who cannot increase urinary potassium excretion.
Pros: Mix with water. Well tolerated. Highly effective.
Cons: Joel notes that patiromer is only available at specialty pharmacies.
Kashlak Pearl: Anecdotally, Joel notes he’s been able to keep patients with advanced CKD and hyperkalemia on an ACEI (or ARB) by using these agents.
Sodium bicarbonate is a slow therapy. Raising the pH lowers the ionized calcium. Hydrogen ions leave albumin and make room for binding of calcium ions. Calcium is stabilizing to the myocardium. For this reason, lowering the ionized calcium (via bicarbonate) is not ideal in the patient with ACUTE hyperkalemia. Joel believes sodium bicarbonate’s main role is in the CHRONIC setting (e.g. Type 4 RTA in a patient with K+ of 5.7 mEq/L).
TMP-SMX blocks the ENac channel. Thus, it impairs distal sodium reabsorption and in turn, potassium excretion. Use of TMP-SMX in combination with other agents that raise potassium has been linked to increased risk for sudden cardiac death [Antoniou CMAJ 2015 – PMC4347789]. Dr Topf reminds us to think twice before prescribing it to patients at risk for hyperkalemia.
Certain foods contain a high amount of potassium phosphate. In practice, Joel doesn’t find this to be a major cause of hyperkalemia since potassium phosphate INCREASES renal excretion of potassium. This is probably why increasing potassium rich foods is ineffective as treatment for HYPOKALEMIA. That said, avoid citrus fruits, tomato juice, kiwis, and dates in patients with potassium elevation. –Dr Topf’s expert recommendation
One study found mortality benefit for potassium supplementation in patients prescribed loop diuretics [Leonard PLoS One 2014 – PMID25029519]. In a re-analysis of the ALL-HAT trial, approx 12 percent of patients on chlorthalidone had hypokalemia after one year. These patients had an increase in mortality [Alderman Hypertension 2013 – PMC3373273].
Kashlak pearl: Joel notes that patients with salt sensitive hypertension might drop their blood pressure just by taking a potassium supplement. Morton’s LITE salt contains potassium chloride granules and is a potential alternative to or potassium supplements! The DASH diet (high potassium and calcium, low sodium) studies cited in JNC 7 found a BP reduction fo 8-14 mmHg.
Listeners will develop a systematic approach to the diagnosis and management of hyperkalemia (elevated potassium) in the acute and chronic setting.
After listening to this episode listeners will…
Dr Topf’s blog lists the following disclosures “I have an ownership stake in a few Davita run dialysis clinics and a vascular access center. Takeda Oncology made a donation to MM4MM the program that is taking me to Mount Everest in 2018”. The Curbsiders were sponsored by ACP’s Internal Medicine Meeting 2019 for this episode.
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dear curbsiders can we keep podcasts in mp3 format? I am sure this podcast is a pearl, most audiobook players in android world arent recognizing this and i end up using audio converter to listen while i drive. thank you
Hi Enrique - iTunes recommends we do a .m4A file, but you should be able to stream on Spotify, Pandora, Overcast, etc.
Good lecture , very informative
I found this a fantastic refresher. Thanks so much for going back to basics in this one. One question, though. I'm looking for the CME/MOC activity on ACPs website, and I can't find it (the last one listed is for #136). Any idea when the MOC quiz will go online?
Thanks for the great feedback! Here is a link to the CME/MOC credit approved episodes: https://www.acponline.org/cme-moc/cme/podcasts/curbsiders Not all of our shows are available for credits, but we usually have at least one per month.