One of my dialysis patients suffers from chronic cryptogenic diarrhea. Because of the diarrhea she does not get volume overloaded or hypertensive. This week I received a call from the dialysis unit telling me she has missed 5 treatments in the first 3 weeks of the month. Sure enough the next day she ends up in the hospital, suffering the effects of chronic uremia. She had a bicarbonate of 4, a BUN of 120, and Cr of 16. Potassium was fine at 3.9 but the phos was 16.8 mg/dL. I don’t think I have seen one that high, outside of rhabdo.
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
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.