1. Description of the problem

What every clinician needs to know

Potassium (K) is a major intracellular cation. Kidneys eliminate 85-90% of daily K excretion. Normal serum K is between 3.5-5.5mEq/L. Hypokalemia is a serum K concentration of less than 3.5mEq/L. Hyperkalemia is a serum concentration of greater than 5.5mEq/L.

Common causes of hypokalemia: G.I. causes (decreased oral intake, nasogastric suction, enteral fistulas, chronic diarrhea and laxative abuse); renal causes (diuretic use, RTAs,); endocrine disorders (DKA, Cushing’s syndrome, primary aldosteronism, Bartter syndrome, magnesium deficiency and thyrotoxicosis); and intracellular K shifts secondary to insulin, beta-2 agonist and hypokalemic periodic paralysis.

Common causes of hyperkalemia: acute or chronic kidney injury, hyporenemic hyperaldosteronism, K sparing diuretics, acute tissue breakdown (crush injury/trauma, burns, major surgery, rhabdomyolysis, cell lysis due to chemotherapy). Another common cause is pseudohyperkalemia secondary to hemolysis of sample either due to difficult blood draw (heel stick) or release of K from platelets during clotting in the sample.

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Clinical features

Hypokalemia affects muscle (skeletal and smooth muscle) as well as the heart. When serum K is less than 3mEq/L EKG changes become apparent (sagging of ST segment, depression of T wave and elevation of U wave). Muscular weakness (first seen in limb, trunk and then respiratory), autonomic dysfunction (orthostatic hypotension and tetany). Paralytic ileus and gastric dilation. Rhabdomyolysis can be caused by hypokalemia.

Hyperkalemia causes muscle weakness (paresthesias followed by weakness and finally flaccid paralysis) and cardiac toxicity. At serum K of 6mEq/L tall T waves appear on EKG, at serum of 7mEq/L the PR interval is prolonged. At higher levels (>8mEq/L) we see absence of P wave, widening of QRS and ultimately the development of ventricular tachycardia/fibrillation. Because of cardiac toxicity hyperkalemia is a medical emergency.

2. Emergency Management

Hyperkalemia is a medical emergency. Emergency treatment involves the protection of the heart (stabilization of the cell membrane potential). This is done using 10% calcium gluconate IV, rapid IV injection of dextrose and regular insulin. Sodium bicarbonate IV may be used, especially in the setting of metabolic acidosis.

Hypokalemia needs to be treated acutely in the setting of hypokalemia induced paralysis, DKA or if there are EKG changes due to hypokalemia. IV KCL can be given (0.5mEq/kg slow over 1 hour).

3. Diagnosis

For hypokalemia a basic metabolic panel (BMP) + other labs ionized ca, serum magnesium and blood pH (blood gas) is required.

For hyperkalemia, in addition to the above labs under hypokalemia, a quick beside istat measurement of serum K (either from a venous line or arterial line) may be useful to rule out pseudohyperkalemia.

EKG maybe useful in both conditions but therapy should not be delayed, especially in hyperkalemia.

4. Specific Treatment

Hypokalemia: mild asymptomatic hypokalemia is treated with oral potassium supplements or IV KCL. A child on chronic diuretic therapy may need chronic supplementation with oral or IV KCL. In certain conditions (EKG changes, paralysis, diabetic ketoacidosis with vomiting), intravenous supplementation may be needed.

Hyperkalemia is a medical emergency and requires a two-pronged approach:

  • Stabilize the cell membrane electrical potential.

  • Acutely lower serum K.

First prong therapy: 10% calcium gluconate IV over 2-3 minutes (repeat in 5 minutes if EKG is still abnormal). Second prong: IV regular insulin with IV 10% dextrose. Continue IV dextrose and monitor serum glucose for hypoglycemia. The data on using inhaled albuterol (beta adrenergic agonist) in children is limited. IV sodium bicarbonate may be used only in the setting of metabolic acidosis. Removal of KCL requires dialysis (usually in setting of renal failure) or use of Kayexalate.

Oral potassium is dosed at 2-5mEq/kg in divided doses (not to exceed 1-2mEq/kg per dose).

IV KCL is dosed at 0.5mEq/kg over 1 hour, not to exceed 20mEq over 1 hour. Frequent reassessment of serum K is necessary before repeat doses of IV KCL are given.

10% calcium gluconate IV 1mg/kg IV over 2-3 minutes (give over 20-30 minutes in setting of digitalis toxicity).

IV regular insulin 0.1u/kg with 3-5ml/kg of IV 10% dextrose.

Na+ bicarbonate IV 1-2mEq/kg.

Kayexalate 1g/kg oral or rectal (preferred as it works faster).

For hypokalemia unresponsive to oral supplementation, IV KCL may be required. K sparing diuretics such as spironolactone (1-3 mg/kg/day in divided doses q6-q12/hr) may be used for a patient on chronic diuretic therapy.

For hyperkalemia unresponsive to medical therapy, especially in setting of acute kidney injury, hemodialysis or CVVH may be needed.


Potassium creates the resting membrane potential of the cell because of its intracellular concentration gradient through the activity of Na/K-ATPase. Hyperkalemia will bring the cell membrane potential closer to the depolarization threshold. This results in cardiac conduction problems and muscle weakness/paralysis.


Good with timely correction and frequent reassessment of serum K.

Special considerations for nursing and allied health professionals.

Do not merely treat “the number,” especially in setting of hypokalemia. Mild asymptomatic hypokalemia with no EKG abnormalities may not require IV therapy as along as serum K is greater than 2.5mEq/L. The danger of giving a wrong dose of IV potassium and killing the patient obviously outweighs the benefit of trying to correct a low number.

What's the evidence?

Evans, K, Greenberg, A. “Hyperkalemia: A review”. J intensive Care Med. vol. 20. 2005. pp. 279-90.

Patiel, O, Salakhov, E, Ronen, L. “Management of severe hypokalemia in hospitalized patients”. Arch Intern Med. vol. 161. 2001. pp. 1089-95.