When acute renal failure is oliguric, distal delivery of sodium and water is low, and hyperkalemia is a frequent problem. What to do? If respiratory status allows, add aggressive volume resuscitation to your medical management. If the patient’s urine output increases, or when acute renal failure is nonoliguric, distal delivery is usually sufficient and hyperkalemia is less of an issue. Concerned about giving IV fluids to an oliguric patient? Medical management is a temporizing measure in the oliguric patient, and hyperkalemia will always be difficult to treat; a fluid challenge might be worthwhile prior to initiating hemodialysis. Urgent dialysis might be hours away, but fluids can be started within minutes.
If hemodynamics allow, I start forced diuresis with high-dose loop diuretics in an attempt to convert to nonoliguria and promote renal potassium excretion. In life-threatening hyperkalemia all is fair, and—once a patient is nonoliguric—hyperkalemia is much easier to manage.
2) A little potassium is not always bad. There is robust evidence supporting the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) in patients with chronic kidney disease with both diabetic and non-diabetic causes. In most patients, according to the National Kidney Foundation’s Clinical Guidelines, the ACE inhibitor or ARB can be continued if the GFR decline over four months is <30% from baseline value and serum potassium is equal to 5.5 mEq/L. The proper way for the inpatient physician to initiate treatment with an ACE inhibitor or ARB is to start at a low dose, with follow-up in one week for a serum potassium measurement and titration of dose as necessary.
3) During my fellowship, I had an attending who would start a discussion with the phrase “I’m just a dumb nephrologist” and then talk for 25 minutes about the physiology of, theories about, and potential therapeutic interventions for just about any type of kidney disease. I prefer a simple approach, too: insulin and dextrose. Why? Because it works well on just about all patients and is quick to administer. Just about every hospital floor in America has a supply of insulin and dextrose on hand. Give the order and, in most cases, the patient is receiving treatment in a matter of minutes.
4) Sodium bicarbonate buffers hydrogen ions extracellularly while shifting potassium intracellularly to maintain electrical neutrality. Sodium bicarbonate should be reserved for cases with severe metabolic acidosis, because effects might be delayed or unreliable, especially in patients with chronic kidney disease.
5) Beta-2 adrenergic agonists drive potassium intracellularly via the Na,K-ATPase mechanism. Albuterol is most commonly used; however, the dosage used by clinicians is frequently insufficient. A dose of albuterol that is 10–20 mg via nebulizer is required, and response time to lowering of potassium might be up to 90 minutes.1
6) I am often asked what ECG changes need to be present before I recommend treatment of hyperkalemia with calcium chloride or calcium gluconate. In a patient without central venous access the concern is that peripheral intravenous infusions of calcium might extravasate, leading to local cellular necrosis and possible loss of limb.
The answer I give is that I don’t know what exact ECG changes would benefit from treatment versus no treatment. In fact, patients with life-threatening hyperkalemia might have subtle changes on ECG.2 Therefore, I believe that every patient with electrocardiographic manifestations of hyperkalemia can be treated with calcium infusion. In my mind, the outcome of sudden cardiac death is far worse than the possible negative effects of calcium infusion.
EKG in patient with hyperkalemia.
7) If you suspect a renal cause for a potassium derangement, please check the urine electrolytes. This test is best done at the time of admission or when the patient is in a steady state. As a practicing nephrologist, I find that most of my consults for electrolyte abnormalities are for the patient with a chronic potassium abnormality. I am usually called on the second or third day, when the patient has received a multitude of IV fluids, treatment, medication changes, and so on. All too often, no urine studies have been obtained at the time of consultation. Would you consult your cardiologist for chest pain without first obtaining an ECG?