Hypokalemia in Emergency Medicine
Practice Essentials
Hypokalemia is defined as a potassium level of less than 3.5 mEq/L, while moderate hypokalemia is a serum level of 2.5-3 mEq/L. Severe hypokalemia is defined as a level of less than 2.5 mEq/L.
Potassium is one of the body's major ions. Nearly 98% of the body's potassium is intracellular. The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. Small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular and neuromuscular systems. [1, 2, 3]
The kidney determines potassium homeostasis, and excess potassium is excreted in the urine.
The reference range for serum potassium level is 3.5-5 mEq/L, with total body potassium stores of approximately 50 mEq/kg (ie, approximately 3500 mEq in a 70-kg person).
Signs and symptoms of hypokalemia
Findings that are consistent with severe hypokalemia may include the following:
Signs of ileus
Hypotension
Ventricular arrhythmias [4]
Cardiac arrest
Bradycardia or tachycardia
Premature atrial or ventricular beats
Hypoventilation, respiratory distress
Respiratory failure
Lethargy or other mental status changes
Decreased muscle strength, fasciculations, or tetany
Decreased or absent tendon reflexes
Cushingoid appearance (eg, edema)
Workup in hypokalemia
Laboratory studies in the workup of hypokalemia include the following:
Serum potassium level [5]
Blood urea nitrogen (BUN) and creatinine level
Glucose, calcium, and/or phosphorus level if coexistent electrolyte disturbances are suspected
Consider digoxin level if the patient is on a digitalis preparation; hypokalemia can potentiate digitalis-induced arrhythmias
Consider arterial blood gas (ABG); alkalosis can cause potassium to shift from extracellular to intracellular
Electrocardiography can reveal the following
T-wave flattening or inverted T waves
Prominent U wave that appears as QT prolongation
ST-segment depression
Ventricular arrhythmias (eg, premature ventricular contractions [PVCs], torsade de pointes, ventricular fibrillation) [4]
Atrial arrhythmias (eg, premature atrial contractions [PACs], atrial fibrillation)
Thyroid screening studies include assessment of thyroid-stimulating hormone (TSH), free triiodothyronine (T3), and free thyroxine (T4) in patients with tachycardia, especially Asian patients [6]
Management
Emergency department management of hypokalemia includes the following:
Patients in whom severe hypokalemia is suspected should be placed on a cardiac monitor; establish intravenous access and assess respiratory status
Direct potassium replacement therapy by the symptomatology and the potassium level; begin therapy after laboratory confirmation of the diagnosis
If patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) have only minor symptoms, they may need only oral potassium replacement therapy; patients with mild hypokalemia whose underlying cause of hypokalemia can be corrected may not need any potassium replacement; if cardiac arrhythmias or significant symptoms are present, then more aggressive therapy is warranted
If the potassium level is less than 2.5 mEq/L, intravenous potassium should be given
The serum potassium level is difficult to replenish if the serum magnesium level is also low; look to replace both
Pathophysiology
Hypokalemia may result from conditions as varied as renal or GI losses, inadequate diet, transcellular shift (movement of potassium from serum into cells), and medications.
Epidemiology
In an Italian study, Giordano et al found that of 7941 emergency department patients, 13.7% of them had an electrolyte imbalance, with hyponatremia being the most common (44%) and hypokalemia being the next most frequent (39%). The investigators also found that 98% of patients with an electrolyte imbalance had an associated systemic disease. [8]
Sex
Incidence is equal in males and females.
Prognosis
Hypokalemia usually resolves with appropriate therapy. However, in the aforementioned study by Singer et al of adult emergency department patients, hyperkalemia and hypokalemia were implicated as risk factors for death, relative to their severity. [7]
Similarly, a study by Krogager et al indicated that patients with hypertension who have a potassium level outside of the 4.1-4.7 mmol/L range, including those who are hypokalemic or hyperkalemic, have an increased mortality risk. For patients with hypokalemia, the 90-day mortality rate was 4.5%, compared with 1.5% for the 4.1-4.7 mmol/L range. [9]
A study by Kieneker et al indicated that not only is hypokalemia linked to the progression of existing chronic kidney disease (CKD), it is also associated with an increased risk of developing CKD, either with or without diuretic use. [10]
A retrospective study by Marill and Miller of emergency department patients indicated that hypokalemia is strongly associated with prolonged heart rate–corrected QT (QTc) duration, particularly in women. The study found that in patients with a potassium level below 3.9 mmol/L, every 1 mmol/L reduction in potassium increased the QTc time by 43.0 ms in women and 29.5 ms in men. [11]
Patient Education
Diet modification is recommended for those patients who are predisposed to hypokalemia. Increase intake of bananas, tomatoes, oranges, and peaches because they are high in potassium. Clinical Presentation
History
The history may be vague. Patients are often asymptomatic, particularly with mild hypokalemia. Symptoms are often due to the underlying cause of the hypokalemia rather than the hypokalemia itself. Hypokalemia should be suggested by a constellation of symptoms that involve the GI, renal, musculoskeletal, cardiac, and nervous systems. The patient's medications should be reviewed to ascertain whether any of them could cause hypokalemia.
Common symptoms include the following:
Palpitations
Skeletal muscle weakness or cramping
Paralysis, paresthesias
Constipation [12]
Nausea or vomiting
Abdominal cramping
Polyuria, nocturia, or polydipsia
Psychosis, delirium, or hallucinations
Depression
Physical
Findings that are consistent with severe hypokalemia may include the following:
Signs of ileus
Hypotension
Ventricular arrhythmias [4]
Cardiac arrest
Bradycardia or tachycardia
Premature atrial or ventricular beats
Hypoventilation, respiratory distress
Respiratory failure
Lethargy or other mental status changes
Decreased muscle strength, fasciculations, or tetany
Decreased or absent tendon reflexes
Cushingoid appearance (eg, edema)
Causes
Renal losses
Renal tubular acidosis
Hyperaldosteronism
Magnesium depletion
Leukemia (mechanism uncertain)
A study by Ravioli et al found dyskalemia not only to be common in emergency department patients with acute kidney injury (AKI), but to independently increase the risk of adverse outcomes. Of patients with AKI admitted to a Swiss public hospital’s emergency department, 11% were determined to have hypokalemia, and 13%, hyperkalemia. Current use of thiazide or loop diuretics, as well as a medical reason for emergency department admission, were risk factors for hypokalemia in patients with AKI, while male gender and the use of potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), or angiotensin-converting enzyme (ACE) inhibitors reportedly protected against hypokalemia. The presence of potassium levels of less than 2.5 mmol/L or greater than 5.0 mmol/L were found to be independently tied to an increased risk of in-hospital mortality. [13]
GI losses (source may be medical or psychiatric, ie, anorexia or bulimia)
Vomiting or nasogastric suctioning
Diarrhea
Enemas or laxative use
Ileal loop
Medication effects
Diuretics (most common cause)
Beta-adrenergic agonists
Steroids
Theophylline
Aminoglycosides
Transcellular shift
Insulin
Alkalosis
Malnutrition or decreased dietary intake, parenteral nutrition
Differential Diagnoses
Workup
Laboratory Studies
Laboratory studies include the following:
Serum potassium level < 3.5 mEq/L (3.5 mmol/L) [5]
BUN and creatinine level
Glucose, calcium, and/or phosphorus level if coexistent electrolyte disturbances are suspected.
Magnesium levels are unreliable and typically do not change management, since patients with hypokalemia almost always have coincident hypomagnesemia and should be treated empirically.
Consider digoxin level if the patient is on a digitalis preparation; hypokalemia can potentiate digitalis-induced arrhythmias.
Consider arterial blood gas (ABG): Alkalosis can cause potassium to shift from extracellular to intracellular.
Imaging Studies
Computed tomography (CT) scanning of the adrenal glands is indicated if mineralocorticoid excess is evident (rarely needed emergently).
Other Tests
Electrocardiography
T-wave flattening or inverted T waves
Prominent U wave that appears as QT prolongation (see the image below) Prominent U waves after T waves in hypokalemia.
ST-segment depression
Ventricular arrhythmias (eg, premature ventricular contractions [PVCs], torsade de pointes, ventricular fibrillation) [4]
Atrial arrhythmias (eg, premature atrial contractions [PACs], atrial fibrillation)
Thyroid screening studies - Thyroid-stimulating hormone (TSH), free T3, and free T4 in patients with tachycardia, especially Asian patients [6]
Treatment & Management
Prehospital Care
Be attentive to the ABCs.
If the patient is severely bradycardic or manifesting cardiac arrhythmias, appropriate pharmacologic therapy or cardiac pacing should be considered.
Emergency Department Care
Emergency department care includes the following:
Patients in whom severe hypokalemia is suspected should be placed on a cardiac monitor; establish intravenous access and assess respiratory status.
Direct potassium replacement therapy by the symptomatology and the potassium level. Begin therapy after laboratory confirmation of the diagnosis.
Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy. Patients with mild hypokalemia whose underlying cause of hypokalemia can be corrected may not need any potassium replacement, such as those with vomiting successfully treated with antiemetics. If cardiac arrhythmias or significant symptoms are present, then more aggressive therapy is warranted. This treatment is similar to the treatment of severe hypokalemia.
If the potassium level is less than 2.5 mEq/L, intravenous potassium should be given. Admission or ED observation is indicated; replacement therapy takes more than a few hours.
The serum potassium level is difficult to replenish if the serum magnesium level is also low. Look to replace both.
Patients should be transferred only after any cardiac arrhythmias have been treated and the condition has been stabilized. Depending on the level of hypokalemia, an advanced cardiac life support (ACLS) ambulance should be used to allow continuous cardiac monitoring during transport.
Consultations
An internist or a nephrologist should be consulted for admission or follow-up care.
Consider psychiatric consultation in laxative abuse, anorexia, or bulimia cases. [14]
Medical Care
Further inpatient care involves continuing intravenous replacement of potassium as needed, cardiac monitoring in severe hypokalemia, and repeating potassium level measurements every 1-3 hours.
Identify the etiology of the hypokalemia.
Consider switching to potassium-sparing diuretic if diuretic therapy is needed. Take 40 mEq KCI daily for 2-3 days and repeat the potassium level.
Complications Replacing potassium too quickly can cause a rapid rise in the blood potassium level, leading to a relative hyperkalemia with subsequent cardiac complications. If hypokalemia is not corrected easily with replacement therapy, search for other coexistent metabolic abnormalities (eg, hypomagnesemia). Hypokalemia may be refractory to treatment until hypomagnesemia is corrected. Hypokalemia can potentiate digitalis toxicity in patients who are taking digoxin.
Medication
Medication Summary
Oral is the preferred route for potassium repletion because it is easy to administer, safe, inexpensive, and readily absorbed from the GI tract. For patients with mild hypokalemia and minimal symptoms, oral replacement is sufficient. For patients who have severe hypokalemia and are symptomatic, both intravenous and oral replacement are necessary. While intravenous potassium dosages of up to 40 mEq/h have been advocated, patients should receive no more than 20 mEq/h IV to avoid potential deleterious effects on the cardiac conduction system. Potassium solutions should never be given as an intravenous push and should be administered as a dilute solution. Higher concentrations of intravenous potassium are damaging to the smaller peripheral veins.
Electrolyte supplements
Class Summary
Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. These agents increase the body's potassium level. In general, 1 mEq/L drop in potassium correlates to a loss of 100-200 mEq of total body potassium. Hypokalemia may result from the movement of potassium into cells without loss of potassium from the body.
Potassium chloride (Klor-Con, K-Dur)
Potassium depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of about 100-200 mEq of potassium from total body store. Available in liquid, powder, or tablet form. Any form may irritate the stomach and cause vomiting. Should be taken with food or after meals to minimize GI discomfort. Oral potassium preparations include 8 mEq KCI slow-release tablets, 20 mEq KCI elixir, 20 mEq KCI powder, 25 mEq KCI tablet. In the symptomatic patient with severe hypokalemia, administer up to 40 mEq/h of the IV preparation. Maintain close follow-up care, provide continuous ECG monitoring, and check serial potassium levels. Higher dosages may increase risk of cardiac complications. Many institutions have policies that limit maximum amount of potassium that can be given per hour.
References
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