Year: 2009

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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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Great article on the two new PSA studies in the NEJM

The New York Times has good coverage of the latest data (US Study, European study) on prostate cancer.

I loved this beat which covers the difference between relative and absolute risk and NNT:

[After discussing the 20% reduction in mortality found in the European study] But in terms of individual risk, even that is not a huge benefit. It means that a man who isn’t screened has about a 3 percent average risk of dying from prostate cancer. If that man undergoes annual P.S.A. screenings, his risk drops to about 2.4 percent.

And there is an important tradeoff. P.S.A. testing increases a man’s risk of being treated for a cancer that would never have harmed him in the first place. The European study found that for every man who was helped by P.S.A. screening, at least 48 received unnecessary treatment that increased risk for impotency and incontinence. Dr. Otis Brawley, chief medical officer of the American Cancer Society, summed up the European data this way: “The test is about 50 times more likely to ruin your life than it is to save your life.”

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William Schwartz, the co-discoverer of SIADH has died

William Schwartz has died.

Every Monday at noon during fellowship we had the fluid and electrolyte conference with Dr. Fred Coe. Dr. Coe has extra-sensory powers for electrolytes. When you presented, you would give just the electrolytes and he would re-create the entire case from the metabolic panel. During the lecture he would ask you to explain a certain pathophysiology and then excoriate you if your thoughts were lazy and poorly organized.

If you ever blamed a poorly characterized hyponatremia on SIADH, Dr. Coe would look at you and ask “If Bartter and Schwartz were here, at this table, right now, and were looking at the same data that you have provided, would they agree that this is SIADH? Would they?”

JASN re-printed the original 1957 article describing SIADH in 2001.

Goodbye Dr. Schwartz, yours are the shoulders we stand-on in the daily grind of clinical nephrology.

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How not to randomize a study

If you are designing a randomized study, make sure you actualize randomize your patients. Schiffl messed this up in his study of daily versus three days a week dialysis, for acute renal failure. Schiffl achieved randomization by alternating eligible patients to three days a week versus daily dialysis. One key aspect about randomization, especially in non-blinded studies, is that the investigators cannot know what arm of the study the patient will be in prior to enrolling the patient. With alternating patients every investigator knows which arm the next patient will end-up in and they can make subtle decisions on the appropriateness of the patient or in how they present the consent form to influence the composition of the study arms.

This comes up, because my fellow sent me a paper on prophylactic dialysis prior to CABG (PDF). From the paper comes this gem:

Repeat after me, “If you know what arm the patient will be in prior to enrolling the patient, you are not running a randomized trial.”

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Urinary anion gap

My fellow remembers the urinary anion gap by saying:

NeGUTive

So a negative urinary anion gap is due to gut losses as opposed to an RTA.

Cute.
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iPhone, Blackberry: Fight!


I have a resident in my Farmington office this month. His primary phone is a Blackberry but he also carries an iPod Touch for medical applications. It’s getting to the point that the battle for the mainstream medical computer platform is the iPhone OS.

iPhone OS 3.0 is another major nail in the coffin of the Blackberry, Palm Pre and Windows. With every revision Apple fills in the holes. The critics are running out of ammunition.
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Highest creatinine I have seen in acute kidney injury

We had a patient earlier this month who presented with a creatinine that was 20 mg/dL on admission and rose to 22 on the repeat. That is the highest creatinine I have ever seen in a patient with acute kidney injury. I have a seen two patients with advanced CKD with creatinines in the mid to high thirties. (34 and 37 mg/dL).

When my fellow described the patient I was sure this was going to be CKD until she mentioned, rather triumphantly, that when she examined the patient she palpated a large bladder. She had a Foley placed and the patient voided 1300 mL of urine in the next hour.
Obstructive uropathy in a woman is cervical cancer until proven otherwise. Sure enough, a subsequent CT scan of the pelvis revealed a pelvic mass which was diagnosed as cervical cancer.
The patient was discharged with a creatinine of 1.9 mg/dL.
A few aspects of the case were interesting and surprising:
  • Obstructive uropathy causes an electrogenic type 1 RTA (hyperkalemic type 1 RTA as opposed to the hypokalemic classic type 1 RTA). Because of the RTA, these patients often have hyperkalemia out of proportion to the degree of renal failure. She was not hyperkalemic and presented with a potassium of 4.6 mEq/L.
  • The patient had a pH of 7.2, bicarbonate of 4 and a pCO2 of 8, giving her a metabolic acidosis and a respiratory alkalosis (predicted pCO2 by Winter’s formula is 14±2). I had been taught that patients cannot blow off CO2 below 14 mmHG. I guess she had super lungs. As best we could tell, the respiratory alkalosis was due to anxiety and resolved the following day.
  • My fellow wanted to give bicarbonate for the metabolic acidosis, but I did not. The pH of 7.2 is fine and the patient was hemodynamically stable. Her total calcium was 4.6 and her phosphorous was 10. I was worried that giving bicarbonate would correct the acidosis which at the time was essential to prevent the hypocalcemia from causing tetany or worse. The acidosis shifts bound inactive calcium to the unbound and active ionized form.