Expert panel consensus on hyperkalemia in emergency department

Clinical Presentation and Diagnosis

Because HK manifests in non-specific symptoms, it is prudent to consider the entire clinical picture when diagnosing or treating patients.

Potassium Hemostasis

The total body potassium is approximately 3000 mEq, 98% of which is stored intracellularly. In normal physiologic conditions, the intracellular potassium concentration is approximately 140 mEq/L whereas the extracellular concentration ranges between 3.5 and 5 mEq/L. This balance of plasma potassium is maintained by active Na-K-ATPase pumps and passive potassium efflux, thus setting the resting membrane potential needed for normal nerve, cardiac, and muscle function.

ECG Manifestations

HK decreases the transmembrane potassium gradient leading to increased potassium conductance and shortening the duration of the action potential. This results in ST-segment depression, peaked T waves, and Q-T interval shortening. As potassium levels rise, prolongation of the PR and QRS duration occurs that leads to a sinewave complex and ultimately to ventricular fibrillation or asystole. Hence it is recommended to obtain an ECG early in the evaluation of patients with HK.

Diagnostic Pitfalls

Not all measures of HK represent the actual potassium concentration. Because aggressive treatment of pseudo-HK is unnecessary and potentially lethal, clinicians must distinguish true HK from pseudo-HK and spurious HK.

Treatment

Acute management recommendations involve a threefold approach: (1) stabilization of the cardiac membranes, (2) redistribution of potassium, and (3) elimination of potassium. Multiple potassium lowering agents are available, and they can be used individually or in combination based on severity of HK or institutional protocol.

Stabilization

Calcium

The effect of potassium on myocytes is counterbalanced by the concurrent calcium concentration. It improves or totally reverses HK-related ECG changes, arrhythmias, or cardiac arrest. The initial dose may be repeated if there is no effect within 5–10 minutes.

Redistribution

Insulin/dextrose

Dextrose (glucose) is administered with insulin to prevent hypoglycemia and subsequent doses may be warranted if hypoglycemia persists.

Beta-2 agonists

Albuterol may be ineffective in some patients, and the mechanism of resistance is not understood. Common side effects are tremor, palpitations, headache, and mild hyperglycemia, which may alleviate insulin-induced hypoglycemia when used simultaneously.

Sodium bicarbonate

Currently, there is insufficient evidence to support the use of intravenous sodium bicarbonate for the acute treatment of HK, and it should be used with caution because it can cause sodium and fluid overload.

Elimination

Loop diuretics

Although loop diuretics are effective at promoting potassium excretion, evidence for use of loop diuretics in the acute management of HK is lacking. These agents may be considered for use as adjuncts in a hyperkalemic emergency.

Hemodialysis

In life-threatening HK, hemodialysis is the best option to reduce potassium effectively, and thus vascular access needs to be established emergently in patients who do not already have one.

Oral binders

Though routinely used in the management of HK in the emergency setting, oral potassium binders have yet to be approved for the emergency treatment of life-threatening HK. The newer binders appear to be safe and current investigations are underway to determine their effectiveness on lowering potassium in the acute setting and the subsequent impact on patient outcomes. Currently available binders are sodium polystyrene sulfonate, patiromer, and sodium zirconium cyclosilicate.

Management Algorithm and Disposition

Patients with K > 5.5 mEq/L and presenting to the ED with acute illness are eligible to enter the algorithm.

Step 1: Because pseudo-HK and spurious HK lead to falsely elevated potassium levels, and many EDs use point-of-care blood testing, which cannot detect hemolysis, it is important to verify the potassium level before starting treatment. Hence, the first step in this algorithm is to assess pretest probability of HK by reviewing medical history (DM, congestive HF, CKD), current medications and laboratory abnormalities; note that an isolated K elevation may signify a spurious result. If the history does not fit with laboratory findings, consider retesting from a fresh blood draw.

Step 2: The next step is to evaluate cardiac involvement. If new changes are found, administer calcium gluconate intravenous 1 g as per the algorithm, and repeat as needed. Calcium gluconate is preferred because calcium chloride carries the risk of tissue necrosis in case of extravasation. However, in the hemodynamically unstable patient, calcium chloride may be preferred because it carries 3 times the amount of elemental calcium than that of the gluconate formulation.

Step 3: Treatment options are based on K levels and categorized into redistribution and elimination. Hemodialysis is the most effective way to eliminate K; however, it may not always be indicated or readily available. While waiting on a definitive treatment plan for HK management or arranging for hemodialysis, medical management is an appropriate option. For redistribution of potassium, intravenous insulin/dextrose, and nebulized albuterol are a mainstay in HK management. Based on a recent Cochrane review, bicarbonate is not indicated in the acute treatment of HK anymore but can still be used in cases of acidosis.28 As for elimination of potassium, oral binders may be helpful in sequestering potassium in the GI tract and have an acceptable safety profile. However, their efficacy in the acute setting (ED or in-patient) is limited and these binders should be used only in patients with a functional GI tract (ie, patients with bowel obstruction or postoperative ileus are not good candidates). Newer binders are preferred over SPS because of their safety profile. Lastly, diuretics have been commonly used to treat HK but there are no studies to show their efficacy or onset of action in the acute setting. Hence, they are not recommended to be used as the sole agent.

Step 4: Reassessment of HK is indicated every 2 to 4 hours because most temporizing agents manifest their maximal effect within 2 hours and are likely wearing off by 4 hours. At this point if K > 6 mEq/L, consider redosing with medications (Step 2) and arranging hemodialysis. If K < 6 mEq/L, consider proceeding to the disposition step.

Disposition: Patients should be frequently assessed for abnormal vital signs, rebound HK, and side effects of medications administered. Hemodynamic instability, persistent new ECG abnormality, and new onset HK should be admitted for further evaluation. Admission should also be considered if HK is recalcitrant to acute treatment or in whom potassium was not eliminated (ie, excreted or dialyzed) but only redistributed. Yet for others, discharge should be considered when all of the following apply: (1) the patient has chronic HK, and a cause for the current exacerbation has been identified and rectified; (2) the patient has stable vital signs and feels well to go home; (3) the patient will have close follow-up, ideally within 24 to 48 hours; and (4) the risks and benefits of discharge have been discussed with the patient.