Tag: hyperkalemia

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Kayexalate: risks and benefits

When I was a fellow I got an opportunity to write the chapter in Intensive Care in Nephrology on Disorders of Potassium Homeostasis.

Dr. Murray, the editor and my fellowship program director, told me that I couldn’t use review articles or text books as references. It was a golden experience. I systematically went through all of the pearls I had collected on potassium and drilled down to the original data.

The primary conclusion I had after months of exploring the stacks of The Crerar was that the wall of knowledge that I had assumed backed up all of our clinical practices was more like a chain link fence with isolated points of solidity but mostly holes. Science could provide a rough outline but too much of medicine is based on conjecture and reasoned guesses.

One of my finds was the near total lack of data showing cation-exchange resins to be effective. In the chapter I wrote:

…Two recent studies have questioned the effectiveness of SPS [sodium polysterene] resins, but until larger studies corroborate these findings, SPS resins remain part of the therapy for acute hyperkalemia. (106, 122, PDF) SPS and sorbitol usage have rarely been associated with intestinal necrosis; whether this is due to sorbital, the resin, or other factors is unclear. (123, 124, 125)

The key table from the Gruy-Kappal article showing the lack of effectiveness of SPS resins

This was actually the revised paragraph. The first draft was much stronger. I railed against the use of kayexylate given the lack demonstrated benefit and the emerging data on the dangers of this medication. I was ready to throw kayexalate on the hyperkalemic trash heep along with bicarbonate. My co-author, John Asplin calmed me down and had me moderated the section. He explained that despite the lack of data, SPS resins have a long history of use and explained that though I have the option of using dialysis, intensivists often find themselves in binds where dialysis is not available and they need an extra-renal method for potassium clearance.

I can appreciate Asplin’s wisdom now. In the last decade I have used SPS resins innumerable times in patients with and without ESRD, though my data is circumstantial I am believer in the effectiveness of this drug. I hope the latest publicity about the purported ineffectiveness of Kayexalate leads to well done large studies rather than a loss of this effective medicine.

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EKGs that will soil your shorts

A long time dialysis patient of ours came to the ED yesterday with the chief complaint of “weakness.”

She had not missed any dialysis in the last week. She had gone to the farmer’s market on Saturday (2 days prior to admission) and had purchased some melon. She ate two melons on Saturday and a third on Monday morning. Additionally, she had potatoes on Saturday night and Sunday morning.
On arrival to the ED this was her initial EKG (click on the image for a larger picture):

The potassium was still pending at this time and no action was taken on those peaked Ts and widened QRS.
Fourteen minutes later the EKG deteriorates to a terrifying sinusoidal pattern:

Potassium was still pending but based on the EKG and history of end-stage renal disease she was given two grams of calcium chloride. The CaCl2 was given via a peripheral line. Calcium chloride should be given only via a central line due to the devastating consequences of extravasation of calcium chloride. However, calcium chloride provides three times the calcium as calcium gluconate and is more effective at squashing hyperkalemic arrhythmias. I aplaud this boldness, as it looks like this patient is about to arrest.
The calcium worked great. A minute later things cool down:
Around this time the potassium came back at 9.4 mmol/L. The patient was then given 4 units of insulin. The low dose is typical of our ED as they tend to be skittish about giving 10 units of insulin to ESRD patients due to concern over symptomatic hypoglycemia. They chased the insulin with an amp of D50 and sixty grams of Kayexalate. The glucose was 84 mg/dL prior to the insulin and D50.
Eighteen minutes later the QRS is down to 128 msec from 168 on the initial EKG:

The patient then went for dialysis for 3.5 hours. Two hours with a zero potassium bath and 90 minutes on a one potassium bath. The potassium the next day was 5.5 mmol/L.

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What’s new in Potassium: sudden cardiac death

As the Nephrology Fellow Network recently covered the etiology of cardiovascular disease in dialyzors is unique from the general public. Use of statins, the foundation of preventative cardiology, has repeatedly failed to prevent cardiovascular vascular disease (CVD) among dialyzors. One reason for this, is the propensity for these patients to die of sudden cardiac death (a lethal heart rhythm requiring a shock of electricity or luck to reverse) rather than acute myocardial infarction (heart attacks). In this study (PDF), from Italy, the investigators found that nearly half of the cardiovascular deaths were due to sudden cardiac death (SCD). The authors retrospectively looked at their data to find risk factors for SCD.

They prospectively looked at 476 patients in 5 Italian hemodialysis units. The cohort was tracked for 3 years and had 167 deaths (35%), 32 due to SCD and 35 due to other CVD. On multivariate analysis they found the following risk factors for SCD:
As important as what was significant, is what was not significant. Left ventricular hypertrophy, heart failure and valvular heart disease, all important risk factors for SCD among non-dialysis patients were not associated with SCD in their cohort.

The most interesting analysis was when they parsed out the day of the week the patients died of SCD. Instead of looking at the absolute day they related the day to the patients dialysis schedule. I have modifed their chart to reflect this, with twin X-axis: one for MWF and another for TTS patients.
The red line indicates how high the bars would be if there was no relationship to the dialysis schedule. The highest risk periods were the 24 hours before dialysis at the beginning of the week and the 24 hours after the dialysis at the beginning of the week. Not dialyzing for the two days over the week-end put patients at risk for SCD both before and after subsequent dialysis.

This sounds like an electrolyte associated complication rather than a uremic toxin because of the risk after dialysis, indicating the change in the toxin, not just the high level, is a risk-factor. This is supported by studies (1, 2) of potassium modeling in which the potassium in the dialysate is lowered sequentially during dialysis. By modeling the potassium, the speed of potassium removal is decreased. This has been shown to decrease pre-mature ventricular contractions (a benign momentary disturbance in the heart rhythm that is being used as a proxy for more serious arhythmias, like SCD. Medicine has gotten in trouble with this proxy in the past so it may not be appropriate.).

Summary: modestly high potassiums are associated increased SCD and the two day dialysis holiday on traditional three day a week dialysis is likewise associated with SCD. Hello daily dialysis!

The lecture on Potassium that this entry was drawn from:

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What’s new with hyperkalemia: EKG changes

Today I did a lecture for the fellows on hyperkalemia. It is interesting that nearly none of the content I use to teach the residents and students is used in a lecture for the fellows. Same subject complete rewrite.

I plan on doing four posts on hyperkalemia from this lecture:

  1. EKG changes
  2. Dialysis patients and hyperkalema
  3. Digoxen toxicity and hyperkalemia
  4. Renal adaptation to ACEi and aldo antagonists in CKD

The lecture started off with the case I blogged about last week with the scary EKG and the potassium of 9.9.


I focused on a well done study (Full Text) by Drs Montague, Ouellette and Buller from Yale. They looked at 90 patients with a potassium grreater than 6 and an EKG done within an hour of the potassium. They excluded hemolyzed specimens and patients with cardiac pacing or other conditions which would mask EKG changes.

They graded all the EKGs according to a prospective criteria and recorded the cardiologists assessment.
The average patient was 73 years old (20-93) and half had acute kidney injury (55%) and half had chronic kidney disease (47%). They did not comment on the degree of overlap between those groups. Half the patients had diabetes (55%). Only 31% were on ACEi and 30% on loop diuretics.

The reading cardiologist documented peaked T waves in only 3 of 90 patients with hyperkalemia. The investigators were able to find peaked T waves in only 29. QRS widening was found in only 6 patients. Of the 52 patients who could have been classified as having “Strict Criteria” (you needed a second EKG after resolution of the hyperkalemia and not everyone in the cohort had a second EKG) only 16 actually met strict criteria.
The authors found EKG criteria to be insensitive predictors of hyperkalemia:

  • Sensitivity of strict criteria: 18%
  • Sensitivity of any EKG change 52%

Interestingly, they found that acidosis decreased the likelihood of finding peaked T-waves.

When they looked at arrhythmias as an outcome, EKG changes continued to be a poor clinical guide. They were not sensitive: only one of the patients who subsequently developed an arrhythmia or cardiac arrest had previously met the strict criteria for EKG changes and only 7 had any T-wave findings at all. This is important because it emphasizes the fact that you can not be reassured by a normal EKG in a patient with hyperkalemia.

The study was unable to look at specificity because all of the patients had hyperkalemia. An earlier study by Wrenn, Slovis and Slovis was able to look at sensitivity and specificity because they did have patients without hyperkalemia in their cohort. They retrospectively reviewed the EKGs of 220 patients with either renal failure (n=133) or hyperkalemia (n=87):

  • Sensitivity: 39%
  • Specificity: 85%

When they restricted the cohort to patients with a potassium over 6.5 the sensitivity rose to 58%.

Take home message: a normal EKG should not rule out hyperkalemia and should not decerase your concearn for impending arrhythmia.

Here is the lecture this post is based on:

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EKG Changes with hyperkalemia

Last week one of our second-year fellows was called into the ER for a potassium of 9.9 mEq/L. The EKG you see above was waiting for him. He arranged for emergent dialysis. In the morning the patients EKG looked like this:

Here is the time line of events:

  • 17:24 Na 128, HCO3 9, Cl 103, BUN 100, Cr 5.6 (no potassium was reported out on the initial labs)
  • 18:06 First EKG done
  • 18:28: K=9.9
  • 18:28: U/A Sp Grav 1.012, pH 5, random drug screen positive for opioids
  • 18:45: ABG 7.05/37/408/10
  • 18:45: urine Na 89, urine Cr 50.5, FENa 4.7%
  • 23:00 initiate dialysis: 2 hours on 1 K bath
  • 01:00 complete dialysis
  • 03:30 Na 140, K 5, Cl 107, HCO3 16, BUN 67, Cr 3.8, Ca 9.1, Phos 6.4, Mg 1.4, CPK 941
  • 03:30 ABG 7.22/40/117
  • 09:20 Na 142, K 4.8, Cl 111, HCO3 15, BUN 63, Cr 3.2
  • 10:00 ABG 7.20/42/96

This patient had AKI due to prolonged decreased po intake along with a loop diuretic and ACEi. The patient initially was anuric but rapidly began to recover and by the next morning was making over 100 mL of urine an hour.

His initial EKG is the best example of a sine wave from hyperkalemia I have ever seen. Below is a cardiac cycle from V4. With a quick glance it may look like a very wide QRS complex with the t wave somewhere to the right of the picture. In reality, the QRS duration is only 176 msec and the large upward thrust is the peaked T wave.


EKG Changes with hyperkalemia

  • Peaked T waves
  • Shortened QT interval
  • Widened QRS
  • Sine wave
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Fluid and Electrolyte lecture at Providence from Tuesday Dec 16

I did a lecture at Providence last week.

I was scheduled to just give a electrolyte lecture without any further guidance. I pulled out two interesting cases I had seen in the last few weeks. Both patients have a non-anion gap metabolic acidosis, but one is hypokalemic and the other is hyperkalemic.

Here is the native Powerpoint files for you to use or edit.

Here is the SlideShare for online viewing

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Great cases on call

I’m running the on-call gauntlet.

I was on call Sat and Sun December 6,7

Sat December 13

Sat and Sun December 20,21

Thursday through Sunday December 25-28

four straight week-ends, with Christmas thrown in for the Jew. Ughh.

That said this week-end has had a few great cases:
  • IgM Cold-agglutinin hemolytic anemia in need of plasmapheresis.
  • Fluconazole induced hyperkalemia
  • Urinary obstruction induced electrogenic type 1 RTA (Hyperkalemic variety of type 1 RTA)
  • Primary hyperaldosteronism induced hypertensive emergency
I’ll elaborate on some (all) of these cases in the next few days.

Happy holidays