Pseudohyperkalemia: the tweetorial

Last week I posted a tweetorial on pseudohyperkalemia due to CLL and a high white blood cell count.

This case peaked with a potassium of 9.5. Pretty frightening, but that was nothing compared to the potassium of 15.5 I saw in 2014. Details here.

I had another case of pseudohyperkalemia in 2011. That one was due to thrombocytosis.

In response to my Tweetorial, Yash Chivate shared a case of pseudohyperkalemia of his own.

Medical management of hyperkalemia

My team was consulted for acute kidney injury (AKI) and hyperkalemia. Before we saw the patient they had already been given the standard, calcium, bicarb, and insulin/glucose cocktail. This had no effect. Potassium went from 6.4 to 6.4.

The patient was still making urine. The AKI was due to emergency surgery with an impressive estimated blood loss (translation: blood loss measured in liters). We gave a liter of NS, 80mg of IV furosemide and 0.2 mg of oral fludrocortisone. Potassium went from 6.4 to 3.4 despite a further increase in the serum creatinine.

Remember to use the kidney for treating hyperkalemia. Even in AKI you can get impressive results.

Renal clearance of potassium is entirely dependent on the cortical collecting duct, specifically the principal cells. It is a multi-step process:

  1. reabsorption sodium down its chemical gradient through eNaC
  2. The chemical gradient to allow sodium resorption is generated and maintained by the Na-K-ATPase
  3. Movement of sodium without an anion(or a cation going in the opposite direction creates a negative charge in the tubular fluid which pulls potassium down an electrical and chemical gradient from the cells into the tubule. This occurs through ROMK and BIGK.

That is how potassium is excreted but, how is potassium regulated? There are two primary components to regulation:

  1. Aldosterone stimulates the transcription of all three transporters (ENaC, Na-K-ATPase, and ROMK) as well as transcribing versions of the proteins which are more active.
  2. Tubular flow. Increased distal sodium delivery provides plenty of sodium to be reabsorbed into the principal cell providing the negative charge, as well as washes away any secreted potassium to maintain the chemical gradient favoring potassium excretion.

The medical management we provided takes care of both aspects of potassium regulation, the furosemide and saline makes sure there is a robust supply of sodium delivered distally and the fludrocortisone makes sure there is ample aldosterone activity to assist with potassium clearance.

#KidneyCON Fluid, Electrolyte, and Acid-Base Workshop

David Goldfarb (@weddellite) and I put on a fluid, electrolyte and acid-base variety show at KidneyCON. The itinerary:

  1. IV fluid taste test
  2. Hypernatremia
  3. Management of calcium phosphate stones: to K-Citrate or not?
  4. Management of chronic hyponatremia, use of DDAVP
  5. Aspirin toxicity
  6. Hyperkalemia

Both of us had a bunch of additional cases that we didn’t get to so be sure to go deep into the presentation files.

Here are the presentation files:

 

 

Pseudohyperkalemia

The highest potassium I have ever seen? That would be 15.5 mEq/L.

It’s not real. It was pseudohyperkalemia from leukocytosis. The patient had chronic lymphocytic leukemia with a white count of 300,000. If you are not familiar with this condition, check out these posts on Renal Fellow Network: Westervelt and Nate. Nice full text references here and here (pdf).

The pseudohyperkalemia merit badge

The first time I saw this was when I was senior resident. I was sleeping in the call room my pager buzzed. It was the oncology floor with a potassium of 9. The patient had CML and was in a blast crisis. His leukocyte count around 100,000. I immediately suspected pseudohyperkalemia and ordered a whole blood potassium from the ABG lab. It was normal so I went back to sleep. The next morning I received an angry call from the Hemo-Onc fellow. The patient was coding and he was furious that I only ordered an ABG instead of treating the hyperkalemia.

I don’t know if the patient coded from hyperkalemia, but I wish that I had gotten out of bed and evaluated the patient. I solved the problem the nurses alerted me to, but if I assessed him, maybe I could of averted an arrest.

Regrets…

Doctors are like the pyromaniac fireman

A patient, on Friday, explained that doctors are like the pyromaniac fireman who when he’s not putting out fires is secretly setting them so he can fight them.

Ridiculous?

Well, on that same day I saw a patient who previously had uncontrolled blood pressure. I had gotten her blood pressure under control with a combination of torsemide, spironolactone, carvedilol and amlodipine. Her office blood pressure  was 123/72 with a heart rate 86. During the visit she told me that she had fallen three times in the last few weeks. Her standing blood pressure was 96/53 with a heart rate of 96. On her previous visit I had extinguished and set a new fire at the same time. Her previous blood pressure had been in the 150s. Controlling her blood pressure was the right thing to do medically but undoubtably it was the cause of her recent falls and my attempt to trim long term morbidity resulted in her being exposed to increased short term morbidity.

Pyro fireman.

Another patient I saw has advanced diabetic nephropathy, CKD stage 4. He needs an ACE inhibitor or an angiotensin receptor blocker to stave off dialysis, unfortunately he cannot tolerate them because of recurrent of hyperkalemia. A few months ago I added a loop diuretic to control edema and hypertension and a couple of weeks ago he returned for a follow-up. His potassium was 4.6 mmol/L. The loop diuretic had increased kaluresis enough that I felt that I had some room to give another trial of renin-angiotensin blockade. Yesterday I received a call informing me of a critically high potassium in this patient.

Pyro fireman

These cases are not limited to clinical medicine, the ACCORD trial tried to determine if normalizing the Hgb a1c in diabetics reduced cardiovascular mortality. Better diabetic control caused increased total mortality.

In OnTarget the combination of an ACE inhibitor and an angiotensin receptor blocker was tested to see if it could reduce cardiovascular events. The  combination was a favorite among nephrologists as a way to stave off dialysis in patients with persistant proteinruia despite single drug renin-angiotensin blockade. Dual blockade was the fashion mostly in response to the subsequently retracted COOPERATE trial. In OnTarget there was significant increase in renal dysfunction with dual ACEi/ARB and a trend toward increased dialysis:

“…whereas the rate was increased in the combination-therapy group, with 65 patients (0.8%) undergoing dialysis”

Pyro fireman, academic style. 
It’s what makes medicine so difficult, the more you try to help your patients the more you expose them to unintended, adverse reactions. I feel that so little of medical education prepares us to balance these competing end-points, how do you judge what is an acceptable risk of hyperkalemia, how do you balance the risk of hypertension versus the risk of orthostatic hypotension?

Hyperkalemia or not

A patient came to the hospital with a swollen arm. The ED suspected a DVT and ordered a doppler ultrasound which confirmed their suspicion. The admission labs included a chem-7 which revealed a potassium of 7. Her creatinine was 1 and she wasn’t taking an ACEi, ARB, aldactone, ketoconazole, or potassium supplements. The ER was surprised and repeated the study and checked an EKG:

Narrow QRS and unimpressive T-waves

The EKG gave no hint of hyperkalemia, though EKG changes are not a sensitive marker for hyperkalemia. The ED gave insulin, glucose and Kayexalate for the lab finding of hyperkalemia. We were consulted to determine the cause of the hyperkalemia. The patient’s past medical history was significant for primary thrombocytosis and during the hospital stay her platelet count rose to over a million.

dats a lot o’platelets

We presumed that his hyperkalemia was actually pseudohyperkalemia due to the high platelet count. Platelets release potassium when they clot and the risk of pseudohyperkalemia rises as the platelet count approaches a million.

You remember this classic NEJM article from 1962. 

We then sent the patients blood to the ABG lab in a heparinized syringe rather than a red top and the potassium normalized. Platelets release potassium when they are activated. By measuring the potassium in whole blood rather than serum, the contribution of platelet activation is prevented. The ABG results are the electrolytes to the far left in the screen-grab below (click to enlarge).

– Posted using BlogPress from my iPad

No Dr. Topf, no EKG changes

On Monday night I was called by one of our fellows regarding a patient in the ED with a potassium of 8.5. They had already given insulin, glucose and kayexalate and the follow-up potassium was 8.1. This is not much improvemnt and less than you typically see. The patient was in acute renal failure with a creatinine of 3 and was anuric.

I asked if the patient had any EKG changes and according to the ER doc the patient had just a touch o’QRS widening. What do you think?

Peaked symmetric T’s

Link for more on EKG changes in hyperkalemia

That night his CPK was 5,000. The next day it rose to 341,680.

Now dat’s a spicy meatball!

– Initially posted using BlogPress from my iPhone

“Hey, is that asystole?” from the introduction of The Checklist Manifesto

Its the first of July so that has me thinking about medical errors. In that vein here is an anecdote from Atul Gawande’s excellent Checklist Manifesto:

He told me about another patient, who was undergoing an operation to remove a cancer of his stomach when his heart suddenly stopped. John remembered looking up at the cardiac monitor and saying to the anesthesiologist, “Hey, is that asystole?” Asystole is total cessation of heart function. It looks like a flat line on the monitor, as if the monitor is not even hooked up to the patient.The anesthesiologist said, ‘A lead must have fallen off,” because it seemed impossible to believe that the patient’s heart had stopped. The man was in his late forties and had been perfectly healthy. The tumor was found almost by chance. He had gone to see his physician about something else, a cough perhaps, and mentioned he’d been having some heartburn, too. Well, not heartburn exactly. He felt like food sometimes got stuck in his esophagus and wouldn’t go down and that gave him heartburn. The doctor ordered an imaging test that required him to swallow a milky barium drink while standing in front of an X-ray machine. And there on the images it was: a fleshy mouse-size mass, near the top of the stomach, intermittently pressing up against the entrance like a stopper. It had been caught early. There were no signs of spread. The only known cure was surgery in this case a total gastrectomy, meaning removal of his entire stomach, a major four- hour undertaking.
The team members were halfway through the procedure. The cancer was out. There’d been no problems whatsoever. They were getting ready to reconstruct the patient’s digestive tract when the monitor went flat-line. It took them about five seconds to figure out that a lead had not fallen off. The anesthesi¬ologist could feel no pulse in the patient’s carotid artery His heart had stopped.
John tore the sterile drapes off the patient and started doing chest compressions, the patient’s intestines bulging in and out of his open abdomen with each push. A nurse called a Code Blue. 
John paused here in telling the story and asked me to suppose I was in his situation. “So, now, what would you do?” 
I tried to think it through. The asystole happened in the midst of major surgery. Therefore, massive blood loss would be at the top of my list. I would open fluids wide, I said, and look for bleeding. 
That’s what the anesthesiologist said, too. But John had the patient’s abdomen completely open. There was no bleeding, and he told the anesthesiologist so. 
“He couldn’t believe it,” John said. “He kept saying, “There must be massive bleeding! There must be massive bleeding!” But there was none. 
Lack of oxygen was also a possibility. I said I’d put the oxygen at 100 percent and check the airway. I’d also draw blood and send it for stat laboratory tests to rule out unusual abnormalities. 
John said they thought of that, too. The airway was fine. And as for the lab tests, they would take at least twenty minutes to get results, by which point it would be too late.
Could it be a collapsed lung—a pneumothorax? There were no signs of it. They listened with a stethoscope and heard good air movement on both sides of the chest. 
The cause therefore had to be a pulmonary embolism, I said—a blood clot must have traveled to the patient’s heart and plugged off his circulation. It’s rare, but patients with cancer undergoing major surgery are at risk, and if it happens there’s not much that can be done. One could give a bolus of epinephrine—adrenalin—to try to jump-start the heart, but it wouldn’t likely do much good. 
John said that his team had come to the same conclusion. After fifteen minutes of pumping up and down on the patient’s chest, the line on the screen still flat as death, the situation seemed hopeless. Among those who arrived to help, however, was a senior anesthesiologist who had been in the room when the patient was being put to sleep. When he left, nothing seemed remotely off-kilter. He kept thinking to himself, someone must have done something wrong. 
He asked the anesthesiologist in the room if he had done anything different in the fifteen minutes before the cardiac arrest. 
No. Wait. Yes. The patient had had a low potassium level on routine labs that were sent during the first part of the case, when all otherwise seemed fine, and the anesthesiologist had given him a dose of potassium to correct it. 
I was chagrined at having missed this possibility An abnormal level of potassium is a classic cause of asystole. It’s mentioned in every textbook. I couldn’t believe I overlooked it. Severely low potassium levels can stop the heart, in which case a corrective dose of potassium is the remedy. And too much potassium can stop the heart, as well—that’s how states execute prisoners. 
The senior anesthesiologist asked to see the potassium bag that had been hanging. Someone fished it out of the trash and that was when they figured it out. The anesthesiologist had used the wrong concentration of potassium, a concentration one hundred times higher than he’d intended. He had, in other words, given the patient a lethal overdose of potassium.
After so much time, it wasn’t clear whether the patient could be revived. It might well have been too late. But from that point on, they did everything they were supposed to do. They gave injections of insulin and glucose to lower the toxic potassium level. Knowing that the medications would take a good fifteen minutes to kick in—way too long—they also gave intravenous calcium and inhaled doses of a drug called albuterol, which act more quickly. The potassium levels dropped rapidly. And the patient’s heartbeat did indeed come back.
The surgical team was so shaken they weren’t sure they could finish the operation. They’d not only nearly killed the man but also failed to recognize how. They did finish the procedure, though. John went out and told the family what had happened. He and the patient were lucky. The man recovered—almost as if the whole episode had never occurred.