Hypokalemia resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] Iqra Qamar M.D.[3]

Overview

Hypokalemia is defined as plasma potassium concentration less than 3.5 mEq/L. Hypokalemia may present as ileus, muscle cramps, rhabdomyolysis, and polyuria. Electrocardiography findings may include U wave, flat or inverted T waves, prolonged QT interval, and ventricular ectopy.

Causes

Life Threatening Causes

Life-threatening conditions which may result in death or permanent disability within 24 hours if left untreated. Severe hypokalemia may be life-threatening and must be treated as such irrespective of the underlying cause.

Common Causes

Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia.

Trans-cellular shifts	Renal loss		GI loss	Increased hematopoiesis	Decreased intake of potassium
Metabolic alkalosis (K+/H+ exchanger) Insulin (activates Na+/K+ ATPase) Catecholamine (activates Na+/K+ ATPase) Hypokalemic thyrotoxic periodic paralysis Hypothermia Chloroquine Barium intoxication Cesium intoxication Antipsychotic overdose	Subject is normo or hypotensive Associated with acidosis Diabetic ketoacidosis Renal tubular acidosis type 1 Renal tubular acidosis type 2 Associated with alkalosis Diuretics Vomiting (increase in aldosterone) Bartter's syndrome (dysfunction of in loop of Henle) Gitelman's syndrome (dysfunction in distal convoluted tubules) Variable acid/base status Hypomagnesemia	Subject is hypertensive Primary hyperaldosteronism Conn's syndrome Secondary hyperaldosteronism Renovascular disease Renin secreting tumor Non aldosterone increase in mineralcorticoid Cushing's disease Congenital adrenal hyperplasia Increased mineralcorticoids Licorice ingestion Liddle's syndrome	Associated with metabolic acidosis Diarrhea Laxative abuse Villous adenoma Associated with metabolic alkalosis Vomiting Nasogastric tube drainage	Megaloblastic anemia Treatment of anemia Crisis of AML	Tea and toast diet Anorexia nervosa Alcoholism

Diagnostic Algorithm

Shown below is an algorithm depicting the possible laboratory findings and their interpretation.

Hypokalemia [K+] < 3.5

Order: ❑ 24 hours urinary K+ (UK) ❑ Transtubular potassium gradient (TTKG)

UK > 25-30 mEq/L/day TTKG > 7

UK < 25 mEq/L/day TTKG < 3

Renal loss of potassium

GI loss of potassium

What is the blood pressure?

Possible etiologies are: Diarrhea Laxatives Villous adenoma

Normal or ↓

↑

Check the acid/base status

Possible etiologies are: Primary aldosteronism Secondary aldosteronism Non aldosterone increase in mineralcorticoids

Acidemia

Alkalemia

Variable

Order: ❑ Aldosterone ❑ Renin

Possible etiologies are: Diabetic ketoacidosis Renal tubular acidosis

Check urinary chloride (UCl)

Hypomagnesemia

↑ Aldosterone ↓ Renin

↑ Aldosterone ↑ Renin

↓ Aldosterone

UCl < 20

UCl > 20

Primary aldosteronism

Secondary aldosteronism

Non aldosterone increase in mineralcorticoids

Possible etiologies are: Vomiting Nasogastric tube

Possible etiologies are: Diuretics Bartter's Gitelman's

Management

• Treat the underlying etiology.

• Potassium repletion for the deficit (for every 1 mEq/L decrease in potassium, there is 200 mEq loss of total body potassium):
  • PO: 40 mEq KCL Q 4-6 hours
  • IV (if urgent): 10 mEq/hour KCL

• Recheck potassium levels in 2-4 hours.

• Provide IV hydration if necessary.

Do's

• Avoid excessive potassium repletion, particularly in the cases of transcellual shifts of potassium that can be reversed when the initial cause of hypokalemia is treated.
• Treat low magnesium blood concentration.

Dont's

• If hydration is needed, do not administer dextrose solutions because dextrose increases insulin which can causes intracellular shift of potassium, and further exacerbates hypokalemia.