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Internal Medicine

Hypokalemia

Introduction

K+ < 3.5 mmol/l

  • One of the m/c water-electrolyte imbalances

Physiology

Potassium homeostasis | Kardalas, E., Paschou, S. A., Anagnostis, P., Muscogiuri, G., Siasos, G., & Vryonidou, A. (2018). Hypokalemia: a clinical update. Endocrine connections, 7(4), R135–R146. https://doi.org/10.1530/EC-18-0109

Aetiology

In general, hypokalemia is associated with diagnoses of cardiac disease, renal failure, malnutrition, and shock. Hypothermia and increased blood cell production (for example, leukemia) are additional risk factors for developing hypokalemia.

Hypokalemia due to potassium depletion:

Hypokalemia can be caused either by decreased intake of potassium or by excessive losses of potassium in the urine or through the GI tract. The latter is more common.
  • Renal losses:
    • Diuretic-induced hypokalemia: Nonpotassium-sparing diuretics
    • Endocrine diseases: Primary hyperaldosteronism
    • Kidney disorders & genetic syndromes affecting the renal function
  • GI losses:
    • Intractable vomiting → Metabolic alkalosis → Hypokalemia
    • Persistent diarrhea → Hypokalaemia + hyperchloremic acidosis
    • Chronic laxative abuse
    • Intestinal obstruction/infections
  • Malnutrition (decreased intake of potassium)

Hypokalemia due to shift of potassium to stores:

  • Insulin administration
  • Stimulation of the sympathetic nervous system
  • Thyrotoxicosis
  • Familiar periodic paralysis
  • Stimulation of Na+/K+-ATPase (Na+/K+ pumps): Catecholamines Beta-adrenoceptor agonists Insulin
HyperaldosteronismEtiologiesReninAldosterone
Primary h.Aldosterone-secreting tumour (usually non-malignant)
Congenital adrenal hyperplasia
Normal or lowHigh
Secondary h.Renovascular disease (eg. Arterial stenosis)
Renin-secreting tumor
HighHigh
PseudoyperaldosteronismCushing’s syndrome
Exogenous mineralocorticoids
Normal or lowNormal or low

Pathophysiology

hypokalemia-clinical-findings
The Calgary Guide | http://calgaryguide.ucalgary.ca/

Hypomagnesemai:

> 50% of clinically significant hypokalemia has concomitant magnesium deficiency and is clinically most frequently observed in individuals receiving loop/thiazide diuretic therapy. Concomitant magnesium deficiency has long been appreciated to aggravate hypokalemia. Hypokalemia associated with magnesium deficiency is often refractory to treatment with K+

Clinical Features

The severity of hypokalemia’s clinical manifestations tends to be proportionate to the degree and duration of serum potassium reduction. Symptoms generally do not become present until serum potassium is below 3.0 mEq/L, unless it falls rapidly or the patient has a potentiating factor, such as the use of digitalis, in which patients have a predisposition to arrhythmias.

Mild hypokalemia: K+ = 3-3.4 mmol/L

Asymptomatic, often diagnosed incidentally during routine blood testing

Moderate hypokalemia: K+ = 2.5-3 mmol/L

Cramping, malaise, myalgia, weakness
  • Ascending muscle weakness
    • Affects lower extremities progressing to involve the trunk and upper extremities and potentially advancing to paralysis
    • GI muscles: Ileus with associated symptoms of nausea, vomiting, and abdominal distension

Severe hypokalaemia: K+ = < 2.5 mmol/L\

Electrocardiogram changes (including ST-segment depression, U-wave elevation, T-wave inversion), arrhythmias, paralysis
  • Musculoskeletal symptoms:
    • Muscle cramps
    • Rhabdomyolysis
    • Resultant myoglobinuria
    • Periodic paralysis: Rare inherited/acquired neuromuscular disorder caused by an acute transcellular shift of potassium into the cells characterized by potentially fatal episodes of muscle weakness/paralysis that can affect the respiratory muscles
  • Cardiac dysrhythmias:
    • ECG changes: T-wave flattening, ST depression and appearance of U wave, PR & QT interval prolongation
asickwalt
Mudlark Tales. (2015). Hypokalemia for dummies. [online] Available at: https://mudlarktales.wordpress.com/2015/02/03/hypokalemia-for-dummies/ [Accessed 1 Apr. 2017]

Case study:


Complications

CVS manifestations:

Arrhythmias associated with hypokalemia can cause following complications:
  • Sinus bradycardia
  • Ventricular tachycardia/fibrillation
  • Torsade de pointes

Prolonged hypokalemia:

Cause structural and functional changes in the kidney that include impairing concentrating ability, increased ammonia production, altered sodium reabsorption and increased bicarbonate absorption.

Glucose intolerance:

Hypokalemia can also result in glucose intolerance by reducing insulin secretion

Respiratory failure and death.

Paralysis of respiratory muscles

Diagnosis

Urinary potassium excretion:

Help distinguish renal potassium losses (e.g., diuretic therapy, primary aldosteronism) from other causes of hypokalemia (e.g., gastrointestinal losses, transcellular potassium shifts)
  • 24-hour urine collection: K+ > 30 mEq/day
  • Spot urine potassium concentration: K+ >15 mmol/L
  • Urine potassium-to-creatinine ratio > 13 mEq/mmol

Assessment of acid–base status:

After determining the presence/lack of renal potassium wasting, assessment of acid-base status should then be determined since some causes of hypokalemia are associated with metabolic alkalosis or metabolic acidosis

Serology:

  • Serum Mg2+ level

ECG:

Although cardiac dysrhythmias or ECG changes are more likely to be associated with moderate to severe hypokalemia, there is a high degree of individual variability and can occur with even mild decreases in serum levels. This variability is dependent on concomitant factors such as magnesium depletion, digitalis therapy, among others.
  • T-wave flattening (first sign)
  • ST depression and appearance of U wave
  • PR & QT interval prolongation

Management

Treatment for hypokalemia focuses on restoring a normal potassium balance, preventing serious complications, and removing or treating the underlying cause(s).3 Management strategies vary depending on the severity of the imbalance.

Potassium replacement therapy:

The goal of potassium replacement in the context of renal or GI losses is to immediately raise serum potassium concentration to a safe level and then replace the remaining deficit over days to weeks.
General Principles of Hypokalemia Management. These steps should be helpful in most cases of hypokalemia; however, clinical judgment should be exercised when applying it to individual patients. Serum potassium levels must be checked no sooner than one hour after an IV dose is given (2 hours after an oral dose). Parenteral potassium should be avoided except in urgent conditions listed and transitioned over to oral preparations as soon as possible. Serum potassium levels should be carefully monitored especially in patients with kidney or cardiac disease. | IV, intravenous; KCl, potassium chloride. Hypokalemia | Asmar, A., Mohandas, R., & Wingo, C. S. (2012). A physiologic-based approach to the treatment of a patient with hypokalemia. American journal of kidney diseases : the official journal of the National Kidney Foundation, 60(3), 492–497. https://doi.org/10.1053/j.ajkd.2012.01.031
TreatmentIndicationMaximum dose/repletion rateMajor side effect
Oral KCLMost patients40 mEq at a time,
once 2-4 h
GI upset
IV KCLNPO, CVS manifestations or K+ < 2.5 mEq/l10 mEq/h via peripheral vein
20 mEq/h via central vein
Burning pain proximal to IV site

Summary

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