The phone rang at 6 a.m. on a cold, stormy winter morning. It was a consult: Would I come see a patient in the ICU? I was in my second year of nephrology fellowship, moonlighting out on the frozen tundra of Minnesota. It was Garrison Keillor country, and—as he says about Lake Wobegon—on that day the woman was strong, but I was one man who was not looking too good. I rolled over and brought up the labs on my bedside computer. The patient’s potassium was 7.8 mmol/L; she also had a creatinine of 6.1 mg/dL, a bicarbonate of 8 mmol/L, and a blood urea nitrogen (BUN) more than 140 mg/dL.
This was a small community hospital with no dialysis facility, and my first thought was that it was time to warm up the Medevac helicopter. I could envision the flight nurses loading the patient and saying, “Welcome aboard Medevac One. Today we will be serving normal saline, insulin, and glucose. Sit back and enjoy the flight, and thank you for choosing Medevac One.” One look outside at the flying snow canceled that plan. I went to see the patient.
One of the first symptoms of uremia is anorexia, and the patient will frequently self-avert from taking protein—sort of a survival mechanism in an attempt to control uremia. I arrived in the ICU to find a woman finishing off a plate of bacon and eggs. She told me she had had a gynecologic procedure done a little over a week before. The pain had been intolerable during the past week. She had not felt like eating or drinking and had been taking a lot of ibuprofen. It was the pain that had brought her to the emergency department, and the narcotics had worked wonders. She was finally feeling well enough to eat. Her ECG was stone-cold unchanged from one obtained pre-operatively.
I treated immediately with intravenous insulin, dextrose, and sodium polystyrene sulfonate. By exam she was volume depleted, and her urine output overnight was less than 10 mL per hour. An arterial blood gas demonstrated a significant mixed acidemia; both anion and nonanion gap acidosis were present. I used a bolus of bicarbonate solution, and the urine output in one hour was 50 mL. This was better, and she had just proven to me that she could make urine. Great news for a nephrologist in training! I ordered a constant infusion of bicarbonate.
Despite these labs, she was hypertensive, so I ordered furosemide—200 mg IV—to attempt a forced diuresis. After another hour, the urine output was 200 mL, and I was much more comfortable. Hyperkalemia is much easier to control when a patient is nonoliguric, and I continued aggressive fluid administration. Within four hours, the patient’s potassium and the acidemia were much improved. By the end of my shift, the potassium was within normal range, the creatinine and BUN had also improved significantly, and the patient was transferred to the medical floor.
This patient’s story illustrates the potential difficulties involved in diagnosing and treating potassium-related problems. With these challenges in mind, here are 10 pieces of information every hospitalist should have when dealing with this type of patient.
1) Hyperkalemia in the patient with acute renal failure is usually a problem of poor perfusion; acute decreases in glomerular filtration rate (GFR) that occur in acute renal failure could lead to a marked decrease in sodium and water at the distal tubule, which might decrease distal potassium secretion.